Gene Annotation
Available parameters and response documentation is available here
GET /lookup/gene/TP53/hg19?add-source-databases=all
{ "gene_id": 33956, "symbol": "TP53", "description": "tumor protein p53", "synonyms": [ "LFS1", "p53" ], "cgd": { "version": "03-Jul-2024", "pub_med_references": [ 1349175, 1565143, 1565144, 1591732, 1679237, 1978757, 3409256, 6016796, 7887414, 8118819, 8718514, 9242456, 10612830, 11219776, 11332399, 11481490, 11498785, 11600572, 12085209, 12524418, 12610779, 12619118, 14583457, 15381368, 15695383, 15741269, 15977174, 18762572, 19171829, 19556618, 19652052, 21056402, 21601526, 21837677, 21946351, 21990040, 22170717, 22551548, 22672556, 22878818, 22939227, 23015295, 23175693, 23355100, 23409989, 23667851, 23894400, 30146126 ], "condition": "Li-Fraumeni syndrome; Choroid plexus papilloma; Ependymoma, intracranial; Osteogenic sarcoma; Breast cancer, familial; Hepatoblastoma; Non-Hodgkin lymphoma; Adrenocortical carcinoma; Colorectal cancer; Bone marrow failure syndrome 5", "inheritance": "AD", "age_group": "Pediatric", "intervention_categories": [ "Oncologic" ], "comments": "Variants may also be involved in susceptibility to a number of types of neoplasms (eg, Basal cell carcinoma, susceptibility to, Glioma, susceptibility to)", "intervention": null }, "civic": { "version": "08-Dec-2023", "items": [ { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Head And Neck Squamous Cell Carcinoma", "doid": "5520", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/517", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a study of 74 patients with head and neck squamous cell carcinoma, those with disruptive mutations in TP53 had shorter overall survival and a higher rate of locoregional recurrence than those without mutations or with nondisruptive mutations.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 22090360 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Deleterious Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Head And Neck Squamous Cell Carcinoma", "doid": "5520", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/518", "evidence_direction": "Does Not Support", "evidence_level": "B", "evidence_statement": "Unlike other studies, in this study of 110 patients with head and neck squamous cell carcinoma, there was no significant difference in the overall survival of patients with and without any TP53 mutations.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 8901856 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Esophagus Squamous Cell Carcinoma", "doid": "3748", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/519", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a retrospective study of patients with esophageal carcinoma, those with mutations in TP53 had worse overall survival.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 19941080 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "B-lymphoblastic Leukemia/lymphoma", "doid": "0080630", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/520", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In children with bone marrow relapsed B-cell precursor acute lymphoblastic leukemia, in multivariate analysis those with mutations in TP53 had worse event-free survival than patients without mutations.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 22699455 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Myelodysplastic Syndrome", "doid": "0050908", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/521", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In patients with myelodysplastic syndrome, in a multivariate analysis those with mutations in TP53 had shorter overall survival than wild-type patients.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 24836762 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Myeloid Neoplasm", "doid": "0070004", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/522", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In patients with myeloma, those with mutations in TP53 had worse overall survival than those without.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 17215851 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Head And Neck Squamous Cell Carcinoma", "doid": "5520", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/523", "evidence_direction": "Does Not Support", "evidence_level": "B", "evidence_statement": "Tumors from 114 patients with head and neck squamous cell carcinoma were analyzed for TP53 mutations, 21 of which were treated with surgery. Unlike those treated with radiotherapy, those treated with surgery did not show a significant difference in rates of loco-regional control between those with and without mutations in TP53.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11325447 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Head And Neck Squamous Cell Carcinoma", "doid": "5520", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/524", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Tumors from 114 patients with head and neck squamous cell carcinoma were analyzed for TP53 mutations. Of the 93 patients treated with radiotherapy, patients with mutations in TP53 had lower rates of loco-regional control and shorter disease-free, disease-specific, and overall survival.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11325447 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Head And Neck Squamous Cell Carcinoma", "doid": "5520", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/525", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In patients with head and neck squamous cell carcinoma, in a multivariate analysis those with truncating mutations in TP53 had worse progression-free and overall survival than wild-type patients.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 21467160 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Truncating Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Head And Neck Squamous Cell Carcinoma", "doid": "5520", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/526", "evidence_direction": "Does Not Support", "evidence_level": "B", "evidence_statement": "In patients with head and neck squamous cell carcinoma, when comparing patients with any mutation in TP53 to wild-type, there was not a significant difference in overall survival in a multivariate analysis.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 21467160 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Truncating Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "B-lymphoblastic Leukemia/lymphoma", "doid": "0080630", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/640", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In relapsed B-ALL patients, TP53 mutations were associated with morphologic nonresponse to therapy (>5% blasts in the bone marrow after 9 weeks of treatment) as well as reduced event free and overall survival when compared to TP53 wildtype patients.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 21747090 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Oral Squamous Cell Carcinoma", "doid": "0050866", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/641", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Oral squamous cell carcinoma patients with TP53 mutations in the DNA binding domain (L2, L3 and the LSH motif) have significantly reduced cumulative survival when compared to patients with TP53 mutations outside of this DNA binding domain. These mutations were also significantly associated with locoregional failure, cervical lymph node metastasis and distant metastasis, likely contributing to this finding.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 12509970 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "DNA Binding Domain Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Gastric Adenocarcinoma", "doid": "3717", "drug_interaction_type": null, "drugs": [ "Chemotherapy" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/850", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In this meta-analysis of 13 studies (564 patients) p53 positivity as defined by high protein expression and/or p53 mutation was associated with improved response to chemotherapy (risk ratio [RR] = 0.704; 95% confidence intervals [CI] = 0.550-0.903; P = 0.006).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 24740294 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Breast Cancer", "doid": "1612", "drug_interaction_type": null, "drugs": [ "Doxorubicin" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/851", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "In this preclinical study, MMTV-Wnt1 mammary tumors with mutant TP53 showed a better clinical response to chemotherapy (doxorubicin) than TP53 wild-type tumors. This was mediated by wild-type TP53-induced cell-arrest under chemotherapy even in the context of heterozygous TP53 point mutations or absence of p21. Thus the status of both TP53 alleles should be assessed because even one copy of wild-type TP53 may contribute to poor response to chemotherapy.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": [ "Doxorubicin" ], "phenotypes": null, "pub_med_references": [ 22698404 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Colorectal Cancer", "doid": "9256", "drug_interaction_type": null, "drugs": [ "Cetuximab", "Oxaliplatin", "Capecitabine" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/875", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In this retrospective biomarker analysis of the EXPERT-C trial, patients with TP53 wild-type status had a statistically significant better progression free survival (PFS) (89.3% vs 65.0% at 5 years; hazard ratio [HR] = 0.23; 95% confidence interval [CI] = 0.07 to 0.78; two-sided P = .02 by Cox regression) and overall survival (OS) (92.7% vs 67.5% at 5 years; HR = 0.16; 95% CI = 0.04 to 0.70; two-sided P = .02 by Cox regression) when treated with Cetuximab + CAPOX (Capecitabine, Oxaliplatin) than in the control arm without Cetuximab.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:33 UTC", "nct_ids": null, "normalized_drug": [ "Capecitabine, Cetuximab, Oxaliplatin" ], "phenotypes": null, "pub_med_references": [ 24957073 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Wildtype", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Esophageal Carcinoma", "doid": "1107", "drug_interaction_type": null, "drugs": [ "Chemotherapy" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/906", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Patients with p53 wild type (as defined by low expression and/or wild-type tp53 gene) had a higher response rate to chemotherapy-based treatment (total major response [MR]: risk ratio [RR] = 1.09, 95 % CI = 1.03-1.16, P = .003; pathological MR: RR = 1.15, 95 % CI = 1.06-1.25, P = .001; total complete response [CR]: RR = 1.08, 95 % CI = 1.00-1.17, P = .040) in this meta-analysis (28 studies, 1497 cases).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:33 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 23515910 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Wildtype", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Acute Myeloid Leukemia", "doid": "9119", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1018", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a study of 97 patients with AML treated with HSCT, 40 had TP53 mutations comprising a total of 44 mutations. Patients with a TP53 mutation had a reduced three year probability of overall survival and event-free survival compared to patients with the wild-type TP53.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 26771088 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Adrenocortical Carcinoma", "doid": "3948", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1028", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "TP53 mutation was shown to be associated with shorter overall survival in patients with adrenocortical tumors (log-rank test; P=0.098). Of 20 patients studied, 5 had coding mutation in TP53. Four of the 5 patients with a TP53 mutation had metastases at diagnosis or detected soon thereafter, and 3 of 4 died of disease within 12 months of surgical resection.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 15922892 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Lung Non-small Cell Carcinoma", "doid": "3908", "drug_interaction_type": null, "drugs": [ "Selumetinib", "Docetaxel" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1145", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A clinical trial comparing selumetinib and docetaxel vs. docetaxel and placebo in KRAS mutant NSCLC was recapitulated in mice. Tumors were induced in lung epithelium by nasal instillation of CRE-bearing adenovirus in conditionally targeted mice. Kras(G12D) and Trp53 knockout mutant mice were resistant to docetaxel monotherapy but sensitive to combined treatment. In a small number of human NSCLC patients with these genotypes FDG-PET signal intensity changes and pERK IHC staining correlated with mouse data.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": [ "Docetaxel, Selumetinib" ], "phenotypes": null, "pub_med_references": [ 22425996 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Lung Non-small Cell Carcinoma", "doid": "3908", "drug_interaction_type": null, "drugs": [ "Docetaxel" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1146", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A clinical trial comparing selumetinib and docetaxel vs. docetaxel and placebo in KRAS mutant NSCLC was recapitulated in mice. Tumors were induced in lung epithelium by nasal instillation of CRE-bearing adenovirus in conditionally targeted mice. Kras(G12D) and Trp53 knockout mutant mice were resistant to docetaxel monotherapy but sensitive to combined treatment. In a small number of human NSCLC patients with these genotypes FDG-PET signal intensity changes and pERK IHC staining correlated with mouse data.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-05-03 22:19:58 UTC", "nct_ids": null, "normalized_drug": [ "Docetaxel" ], "phenotypes": null, "pub_med_references": [ 22425996 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Loss", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Lung Non-small Cell Carcinoma", "doid": "3908", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1147", "evidence_direction": "Does Not Support", "evidence_level": "B", "evidence_statement": "Pooled analysis of TP53 mutations (exons 5-8) from 4 randomized trials (IALT, JBR10, CALGB-9633 and ANITA). Mutations (434; 36%) had no prognostic effect (OBS: HROS=0.99; [95%CI 0.77-1.28], p=0.95; HRDFS=0.99 [0.78-1.25], p=0.92) but were marginally predictive of benefit from ACT for OS (test for interaction: OS: p=0.06; DFS: p=0.11).", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 26899019 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Deleterious Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Lung Non-small Cell Carcinoma", "doid": "3908", "drug_interaction_type": null, "drugs": [ "Adjuvant Chemotherapy" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1148", "evidence_direction": "Does Not Support", "evidence_level": "B", "evidence_statement": "Pooled analysis of TP53 mutations (exons 5-8) from 4 randomized trials (IALT, JBR10, CALGB-9633 and ANITA) of platinum-based adjuvant chemotherapy (ACT) versus observation (OBS). Patients with TP53wt had significantly better PFS and OS with ACT vs. OBS (p=0.005, p=0.02, respectively) whereas patients with TP53 mutations did not show significant differences in PFS and OS between ACT and OBS (p=0.86, p=0.63).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 26899019 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "Deleterious Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Lung Non-small Cell Carcinoma", "doid": "3908", "drug_interaction_type": null, "drugs": [ "Adjuvant Chemotherapy" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1149", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Pooled analysis of TP53 mutations (exons 5-8) from 4 randomized trials (IALT, JBR10, CALGB-9633 and ANITA, 1209 patients, median follow-up 5.5 years) of platinum-based adjuvant chemotherapy (ACT) versus observation (OBS). Patients with wild-type TP53 had better outcomes with ACT than OBS (HROS=0.77 [0.62-0.95], p=0.02; HRDFS=0.75 [0.62-0.92], p=0.005).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:33 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 26899019 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Wildtype", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Sarcoma", "doid": "1115", "drug_interaction_type": null, "drugs": [ "Pazopanib" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1170", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "19 advanced sarcoma patients treated with pazopanib were retrospectively assessed for mutations associated with response using the Foundation one sarcoma/heme panel. Progression-free survival (PFS) of patients with TP53 mutations (all predicted to be loss of function) was significantly greater than TP53 wild-type tumors with the median PFS of 208 versus 136 days, respectively [P = 0.036, hazards ratio 0.38 (95% confidence interval 0.09-0.83)].", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": [ "Pazopanib" ], "phenotypes": null, "pub_med_references": null, "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "Deleterious Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Chronic Lymphocytic Leukemia", "doid": "1040", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1450", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "A study of 53 patients with B-CLL found a significant resistance to chemotherapy and corresponding poor clinical outcomes among the 7 treated patients with p53 mutations compared to the 29 treated patients without.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 8241511 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Chronic Lymphocytic Leukemia", "doid": "1040", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1451", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a study of 126 patients with long-term follow-up, TP53 mutations were significantly associated with shorter median survival in patients (P = 0.002) from time of diagnosis. The median survival from the time of first observation of a TP53 mutation was much more pronounced (P = <0.001). These findings were statistically independent of 17p deletions.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 18689542 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Chronic Lymphocytic Leukemia", "doid": "1040", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1452", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "The authors analyzed 328 patients with CLL, of which 28 were identified to have TP53 mutations. Patients with TP53 mutations were found to have significantly shorter progression-free (HR = 3.8; P < 0.001) and overall survival (HR = 7.2; P < 0.001).", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 20697090 ], "rating": "5", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Chronic Lymphocytic Leukemia", "doid": "1040", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1478", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In the CLL4 trial assessing first line treatment with chlorambucil or fludarabine with or without cyclophosphamide, patients with TP53 mutations experienced poorer overall response rates (27% vs 83%), shorter progression free survival (5 year PFS 5% vs 17%), and overall survival (20% vs 59%) compared to patients without TP53 mutations.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 21483000 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Chronic Lymphocytic Leukemia", "doid": "1040", "drug_interaction_type": null, "drugs": [ "Alemtuzumab" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1481", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Thirty-six patients with CLL were treated with alemtuzumab. Partial or complete response was achieved in 6 of 15 patients with p53 mutations, compared to 4 of 21 without. These findings are not statistically significant, but the authors suggest that alemtuzumab is an effective therapy for patients with p53 mutations or deletions.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": [ "Alemtuzumab" ], "phenotypes": null, "pub_med_references": [ 14726385 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Chronic Lymphocytic Leukemia", "doid": "1040", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1485", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a multivariate analysis of 774 CLL patients, TP53 aberrations were significantly correlated with shorter time to first treatment (HR=2.081; 95% CI=1.431-3.021). This finding was independent of IGHV mutation status.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 24943832 ], "rating": "5", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Chronic Lymphocytic Leukemia", "doid": "1040", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/1507", "evidence_direction": "Supports", "evidence_level": "A", "evidence_statement": "In a cohort of 406 patients with CLL, those patients with clonal or sub-clonal mutations in TP53 had significantly shorter overall survival (HR: 1.71; 95% CI: 1.28-2.26; P = .0001).", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 26837699 ], "rating": "5", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Ovarian Cancer", "doid": "2394", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2697", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "p53 overexpression (>10% positive stained nuclei) was found in 110 cases from a 178 patient cohort with invasive ovarian carcinoma who had undergone surgery. Overexpression of p53 was correlated with poor differentiation (p<0.001) and high S-phase fraction (p<0.001).", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11595686 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Overexpression", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Ovarian Cancer", "doid": "2394", "drug_interaction_type": null, "drugs": [ "Cisplatin", "Carboplatin" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2771", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a group of patients with invasive ovarian carcinoma who had undergone surgery, a subset of 74 patients treated with platinum based chemotherapy were assessed for p53 alteration (p53 mutation or p53 overexpression by immunostaining >10% positive). Significant decreased time to progression (p=0.037) was seen in the subset of patients with p53 alteration (n=54) in comparison to the group with normatl p53 (n=20)", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": [ "Carboplatin, Cisplatin" ], "phenotypes": null, "pub_med_references": [ 11595686 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "ALTERATION", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Breast Cancer", "doid": "1612", "drug_interaction_type": null, "drugs": [ "Tamoxifen" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2783", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a study 202 breast cancer patients undergoing first line tamoxifen treatment, 65 patients had mutations in TP53. Among the p53 wild type population a 66% response rate was reported, where response was considered as complete response, partial response or stable disease. In a patient subgroup with mutations in p53 amino acids that directly interact with DNA, 2 of 11 (18%) of patients responded to tamoxifen.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": [ "Tamoxifen" ], "phenotypes": null, "pub_med_references": [ 10786679 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "DNA Binding Domain Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Breast Cancer", "doid": "1612", "drug_interaction_type": null, "drugs": [ "Tamoxifen" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2784", "evidence_direction": "Supports", "evidence_level": "C", "evidence_statement": "In a study 202 breast cancer patients undergoing tamoxifen treatment, a higher frequency of wildtype TP53 patients responded to treatment compared to those with mutations in TP53 (66% wild-type vs. 31%, odds ratio (OR):0.22, 95CI:0.12-0.42, P<0.0001, univariate analysis; OR:0.29, 95% CI:0.12-0.42, P=0.0014, multivariate analysis). The median survival after start of therapy was shorter in patients with mutations in TP53 than for patients with wild-type TP53 (20mo vs. 29mo, HR:1.99,95% CI:1.43-2.75, P<0.001). Breast cancer patients with TP53 mutations also had a decrease in progression-free survival (HR:2.61, 95% CI:1.90-3.6, P<0.001).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": [ "Tamoxifen" ], "phenotypes": null, "pub_med_references": [ 10786679 ], "rating": "1", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Stomach Cancer", "doid": "10534", "drug_interaction_type": null, "drugs": [ "Etoposide", "Mitomycin", "Cisplatin" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2799", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a Phase II trial of 25 patients with metastaic gastric cancer, patients received preoperative high dose chemotherapy (HDCT) consisting of etoposide, cisplatin and mitomycin. Patients with greater than 50% regression in response to HDCT received surgery. TP53 overexpression was assayed by immunohistochemistry. 14 patients showed p53 overexpression, and 12 of these qualified for resection. Overall survival in patients with p53 overexpression was 17.3 months in contrast to patients with negative p53 immunohistochemistry, where it was 7.2 months (p=0.0003).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": [ "Cisplatin", "Etoposide", "Mitomycin" ], "phenotypes": null, "pub_med_references": [ 14514923 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Overexpression", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Stomach Carcinoma", "doid": "5517", "drug_interaction_type": null, "drugs": [ "Doxorubicin", "Cisplatin", "Etoposide" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2820", "evidence_direction": "Supports", "evidence_level": "C", "evidence_statement": "In a study of 25 patients with advanced gastric cancer, mutations in TP53 were identified in 32% of primary tumors. TP53 mutations were associated with an improved response to preoperative treatment of a modified EAP protocol (combination of doxorubicin, etoposide and cisplatin). Patients with mutations in TP53 had an increased median survival compared to patients with wildtype TP53 (18.5mo vs. 10.2mo, P=0.044).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": [ "Cisplatin", "Doxorubicin", "Etoposide" ], "phenotypes": null, "pub_med_references": [ 14514923 ], "rating": "1", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Cancer", "doid": "162", "drug_interaction_type": null, "drugs": [ "Rebemadlin" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2963", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "MDM2 Inhibitor Nutlin-3a induced senescence in presence of functional TP53 in murine primary fibroblasts, oncogenically transformed fibroblasts, and fibrosarcoma cell lines. Cells lacking functional TP53 were completely insensitive to the drug.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:33 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 17671205 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Wildtype", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Cancer", "doid": "162", "drug_interaction_type": null, "drugs": [ "MDM2 Inhibitor AMGMDS3" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2964", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "MDM2 Inhibitor screen in a panel of 260 cancer cell lines with well characterized TP53 status shows that only cancer cell lines with unaltered TP53 may be sensitive to MDM2 Inhibitor.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:33 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 25730903 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Wildtype", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Leukemia", "doid": "1240", "drug_interaction_type": null, "drugs": [ "RG7112" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2965", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Phase I Trial of RG7112 in 116 heavily pretreated patients with AML, ALL, CML, CLL, sCLL demonstrated sustained clinical improvement and induction of TP53 target genes in subset of patients with wild type TP53. 96 patients were tested for TP53 mutation and 19 cases of mutation were detected. No sustained clinical improvement or induction of TP53 target genes was observed in patients with mutant TP53.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:33 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": null, "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Wildtype", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Leukemia", "doid": "1240", "drug_interaction_type": null, "drugs": [ "RG7112" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2966", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Phase I Trial of MDM2 inhibitor RG7112 in 116 patients with AML, ALL, CML, CLL, sCLL demonstrated sustained clinical improvement and induction of TP53 target genes in subset of patients with wild type TP53. No sustained clinical improvement or induction of TP53 target genes was observed in patients with mutant TP53.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": null, "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Deleterious Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Cancer", "doid": "162", "drug_interaction_type": null, "drugs": [ "MDM2 Inhibitor AMGMDS3" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2967", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "MDM2 Inhibitor screen in a panel of 260 cancer cell lines with well characterized TP53 status shows that only cancer cell lines with unaltered TP53 may be sensitive to MDM2 Inhibitor AMGMDS3, while those with p53 mutations demonstrated resistance.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 25730903 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Deleterious Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Cancer", "doid": "162", "drug_interaction_type": null, "drugs": [ "Rebemadlin" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2968", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "MDM2 Inhibitor Nutlin-3a induced senescence in presence of functional TP53 in murine primary fibroblasts, oncogenically transformed fibroblasts, and fibrosarcoma cell lines. TP53 mutant cells lacking functional TP53 were completely insensitive to the drug.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 17671205 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "Deleterious Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Ovarian Cancer", "doid": "2394", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2993", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Patients with conserved domain p53 mutation (n=61) were compared with those with wild type or non-conserved domain p53 mutation (n=117) in a cohort of 178 invasive ovarian carcinoma patients who had undergone surgery. Overall survival was decreased in the cohort with conserved domian mutation (p=0.005). Conserved domain mutation was an independent factor in univariate (but not multivariate) analysis of overall survival with relative risk 1.70 (1.17-2.47, p<0.007).", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11595686 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "CONSERVED DOMAIN MUT", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": null, "disease": "Lung Non-small Cell Carcinoma", "doid": "3908", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/2999", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "A pooled analysis to investigate the prognostic and predictive roles of TP53/KRAS and TP53/EGFR comutations (cm) in randomized trials of adjuvant chemotherapy compared to observational therapy encompassing a total of 3,553 patients. TP53/KRAS cm showed no prognostic effects but a borderline predictive effect (p=0,04) for negative effect of chemotherapy as compared to tp53/KRAS wt/wt. TP53/EGFR cm in was neither prognostic ( P = .83), nor significantly predictive ( P = .86). Similar results were observed for both groups for disease-free survival.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 28453411 ], "rating": "5", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Ovarian Cancer", "doid": "2394", "drug_interaction_type": null, "drugs": [ "Cisplatin", "Carboplatin" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/3013", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a study involving patients with invasive ovarian carcinoma who had undergone surgery, a subset of 73 patients were classified via response to platinum-based chemotherapy as sensitive or resistant/refractory and tested for p53 overexpression (>10% postive stained nuclei). 78% of p53 negative patients were classified as sensitive, in compariston to 39% of p53 positive patients (p=0.001).", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": [ "Carboplatin, Cisplatin" ], "phenotypes": null, "pub_med_references": [ 11595686 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Overexpression", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Ovarian Cancer", "doid": "2394", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/3014", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In a study of invasive ovarian carcinoma patients who had undergone surgery, the p53 alteration variant was defined as p53 mutation or p53 overexpression by immunostain (>10% positive). Patients with p53 alterations showed increase in poor tumor cell differentiation (p<0.001) and increase in tumor cellular S-phase fraction (p<0.001). Out of 178 patients, p53 alteration (n=132) was associated with decreased overall survival in comparison to normal p53 (n=46), p=0.007.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11595686 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "ALTERATION", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Cancer", "doid": "162", "drug_interaction_type": null, "drugs": [ "MDM2 Inhibitor AMGMDS3" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/4888", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Subset of 58 cancer cell lines with unaltered TP53 is sensitive to MDM2 Inhibitor AMGMDS3. None of 115 cancer cell lines with TP53 mutation and absence of WT allele are sensitive to MDM2 Inhibitor. TP53 R249S loss of function mutation is present in 1 cell line and it is insensitive to MDM2 Inhibitor AMGMDS3.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:47 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 25730903 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "R249S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Resistance", "disease": "Cancer", "doid": "162", "drug_interaction_type": null, "drugs": [ "MDM2 Inhibitor AMGMDS3" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/4889", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Subset of 58 cancer cell lines with unaltered TP53 is sensitive to MDM2 Inhibitor AMGMDS3. None of 115 cancer cell lines with TP53 mutation and absence of WT allele are sensitive to MDM2 Inhibitor. TP53 R280K loss of function mutation is present in 1 cell line and it is insensitive to MDM2 Inhibitor AMGMDS3.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:47 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 25730903 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "R280K", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Neomorphic", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/7531", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "The R282W mutation was used to create isogenic AML cell lines using MOLM13 and K526 lines. R282W/- cells showed resistance to chemotherapeutic agents and failure to induce p21, indicating disruption of p53 function. ChIP assays demonstrated reduced p53 occupation across the genome for most p53 variants tested, while R282W cells indicated mutant p53 neomorphic binding at sites not occupied by wt. RNAseq studies determined that a novel gene expression program was not induced in R282W cells at baseline or with DNA damage induced p53 signal activation, and that the signature of gene expression was most similar to that of p53 loss, indicating that R282W mutation does not induce a neomophic p53 function.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:40 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 31395785 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "R282W", "variant_civic_url": null, "variant_origin": "Unknown", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Sensitivity/Response", "disease": "Solid Tumor", "doid": null, "drug_interaction_type": null, "drugs": [ "Pazopanib", "Vorinostat" ], "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/7540", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "Patients with a hotspot TP53 mutation had a higher rate of SD ≥6 months/PR, longer median PFS, and median OS compared to patients without a hotspot TP53 mutation. Mutations observed in this study include loss of function (A159fs, R213*, and DNA-binding domain truncation) or gain of function (R175H, H179R, H193R, V216M, G245S, and R273C). These mutations were seen in 11 of 36 patients in enrolled in the clinical trial.", "evidence_status": "accepted", "evidence_type": "Predictive", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-11-23 19:14:39 UTC", "nct_ids": [ "NCT01339871" ], "normalized_drug": [ "Pazopanib", "Vorinostat" ], "phenotypes": null, "pub_med_references": null, "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Medulloblastoma SHH Activated", "doid": "0080703", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/8347", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "In the childhood (≥4.3 years) SHH-MB subgroup, TP53 mutations (n=13) are associated with shorter progression-free survival (PFS) compared to the no mutation group (n=35) (HR, 3.47; 95% CI, 1.29 to 9.3; p<0.014).", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:30 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 28545823 ], "rating": "5", "representative_transcript": null, "transcripts": null, "variant": "Mutation", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Renal Wilms' Tumor", "doid": "5176", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/8945", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "44 archival FFPE samples from confirmed cases of Wilms tumor with mean age 3 years 2 months, and taken from the most histologically aggressive parts of each tumor, were stained with p53 monoclonal antibody and the corresponding patient clinical data was analyzed. 24 samples were p53 positive, and did not correlate with age or sex. All tumors with unfavorable histology were p53 positive, in contrast to 13 of 33 tumors with favorable histology, with weak-moderate p53 signal (p<0.001). 2 year overall survival rate was 89.2% in p53 negative, and 55.7% for p53 positive cases (P = .01), and mean survival was 46 months in p53 negative and 26 months in p53 positive cases (P = .02). Compared with p53 negative, tumors with week to moderate p53 signal had HR 3.75 (P = .05), and high signal had HR 8.61 (P = .01). No significant correlation was seen between tumor clinicopathological stage and p53 expression.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 21525573 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Overexpression", "variant_civic_url": null, "variant_origin": null, "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Gain of Function", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/9285", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "In a pre-clinical study, wild-type and P250L TP53 were transiently overexpressed in the human osteosarcoma SaOS-2 cell line, which lacks endogenous p53. Immunofluorescence revealed that the P250L mutant cell line had reduced nuclear and increased cytoplasmic staining as compared to the wildtype. The punctate staining suggested that the P250L mutant forms large aggregates within the perinucleus. Chemical disruption of the microtubule assembly resulted in a shift from punctate to diffuse cytoplasmic staining in the P250L cell line. The oligomerization state of the wild type and P250L p53 was analyzed using Blue-Native PAGE (BN-PAGE) and western blot analysis: It was found that the wild type p53 appeared as monomers, tetramers and octamers while the P250L p53 formed large masses. More importantly, it was found that the formation of these aggregates by the P250L mutant could lead to co-aggregation of the wild-type p53, causing dominant negative activity. Additionally, the P250L mutant was found to inactivate the p53 paralogs, p63 and p73, while upregulating HSP70 and HSP90.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:07 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 21445056 ], "rating": "5", "representative_transcript": null, "transcripts": null, "variant": "P250L", "variant_civic_url": null, "variant_origin": "Unknown", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Poor Outcome", "disease": "Rhabdomyosarcoma", "doid": "3247", "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/9594", "evidence_direction": "Supports", "evidence_level": "B", "evidence_statement": "This study evaluated 641 cases of rhabdomyosarcoma (RMS) that were enrolled in the Children’s Oncology Group (COG) trials from 1998 to 2017 and the UK malignant mesenchymal tumor and RMS2005 trails from 1995 to 2016. Molecular testing included 39 genes which had been implicated in the past with regards to RMS. The analysis was performed with a custom-capture sequencing assay. Altered TP53 was noted in 69 out of 515 FOXO1 fusion-negative RMS cases (13%), with the most frequent mutations at codons G245S (6 cases), R248Q or W (6 cases), R175H (4 cases), and P72A (4 cases). These cases displayed a worse event free survival. In FOXO1 fusion-positive RMS subtype, there was a small number of cases with altered TP53 (3 and 2 cases in the COG and UK patient cohorts, respectively), but they were universally fatal. Due to lack of a matched germline sample, it could not be determined whether the TP53 abnormalities were of somatic or germline origin. Nevertheless, both cohorts show that mutations in TP53 are associated with a poor prognosis in both fusion-negative and fusion-positive RMS, with a particularly bleak outcome in fusion-positive RMS.", "evidence_status": "accepted", "evidence_type": "Prognostic", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:44 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": [ "Pediatric onset", "Young adult onset" ], "pub_med_references": [ 34166060 ], "rating": "4", "representative_transcript": null, "transcripts": null, "variant": "ALTERATION", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Loss of Function", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/9805", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Cancer-associated TP53 mutations were assessed for effects on the stability and oligomeric structure of p53. TP53 R324P protein eluted as a single peak contemporaneously with the known monomer mutant L330A, and separate from tetrameric TP53, during gel-filtration chromatography. The introduction of Proline at the solvent-exposed residue R342 inhibited tetramer formation resulting in p53 remaining in an unfolded monomeric state. Since formation of a tetramer is important for p53 function, destabilization of the tetrameric structure is likely to result in loss of p53 tumor suppressor activity.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:10 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 20978130 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "R342P", "variant_civic_url": null, "variant_origin": "Unknown", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Loss of Function", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/9808", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Cancer-associated TP53 mutations were assessed for effects on the stability and oligomeric structure of p53. TP53 R337P protein eluted as a single peak contemporaneously with the known monomer mutant L330A, and separate from tetrameric TP53, during gel-filtration chromatography. The introduction of Proline at residue R337 in the hydrophobic core inhibited tetramer formation resulting in p53 remaining in an unfolded monomeric state. Since formation of a tetramer is important for p53 function, destabilization of the tetrameric structure is likely to result in loss of p53 tumor suppressor activity.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:10 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 20978130 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "R337P", "variant_civic_url": null, "variant_origin": "Unknown", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10215", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant P98S was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:11 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "P98S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10216", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant P98L was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:11 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "P98L", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10217", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant Y126D was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:11 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Y126D", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10218", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant Y126S was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:11 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Y126S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10219", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant K139E was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:11 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "K139E", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10224", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant I162F was classified as recessive for RGC and a hotspot for mutation (P < 0.014) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:11 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "I162F", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10225", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant Y163H was classified as recessive for RGC and a hotspot for mutation (P < 0.001) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:11 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Y163H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10226", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant Y236S was classified as recessive for RGC and a hotspot for mutation (P < 0.01) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Y236S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10227", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant L252F was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "L252F", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10228", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant E258K was classified as recessive for RGC and a hotspot for mutation (P < 0.01) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "E258K", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10229", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant G262D was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G262D", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10230", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant G266R was classified as recessive for RGC and a hotspot for mutation (P < 0.001) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G266R", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10231", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant G266E was classified as recessive for RGC and a hotspot for mutation (P < 0.001) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G266E", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10233", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant P278S was classified as recessive for RGC and a hotspot for mutation (P < 0.001) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "P278S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10234", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "CAUTION: This Evidence Item has not been accepted as accurate or complete! A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant L308M was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "L308M", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10235", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "CAUTION: This Evidence Item has not been accepted as accurate or complete! A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC sequence as a p53 binding site. TP53 variant L323P was classified as recessive for RGC and was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "L323P", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10236", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant Q144P was classified as recessive for p21, bax, and PIG3. In addition, Q144P was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Q144P", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10238", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant P219H was classified as recessive for p21, bax, and PIG3. In addition, P219H was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "P219H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10239", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant Y220H was classified as recessive for RGC, p21, bax, and PIG3. In addition, Y220H was classified as a hotspot for mutation (P < 0.001) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Y220H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10240", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant E224K was classified as recessive for RGC, p21, bax, and PIG3. In addition, E224K was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "E224K", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10241", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant Y234H was classified as recessive for RGC, p21, bax, and PIG3. In addition, Y234H was classified as a hotspot for mutation (P < 0.001) by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "Y234H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10242", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant T230S was classified as recessive for RGC, p21, bax, and PIG3. In addition, T230S was not classified as a hotspot for mutation by the authors.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "T230S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10243", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant H168Y was classified as dominant negative for p21, bax, and PIG3. In addition, H168Y was classified as a hotspot for mutation (P < 0.014) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "H168Y", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10244", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant P177S was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, P177S was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "P177S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10245", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant P177F was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, P177F was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "P177F", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10246", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant P177H was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, P177H was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "P177H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10247", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant H179Y was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, H179Y was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "H179Y", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10248", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant N239S was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, N239S was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "N239S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10250", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant S241F was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, S241F was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:02 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "S241F", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10252", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant G244S was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, G244S was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G244S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10254", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant G245D was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, G245D was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G245D", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10255", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant M246L was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, M246L was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "M246L", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10257", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant V274F was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, V274F was classified as a hotspot for mutation (P < 0.014) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "V274F", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10258", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant G279E was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, G279E was not classified as a hotspot for mutation by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G279E", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10259", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant D281N was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, D281N was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "D281N", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10260", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant D281E was classified as dominant negative for RGC, p21, bax, and PIG3. In addition, D281E was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "D281E", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10265", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant R156P was classified as recessive for RGC, p21, and PIG3, but it was classified as dominant negative for bax. In addition, R156P was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "R156P", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10268", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant R181H was classified as recessive for RGC, p21, and PIG3, but it was classified as dominant negative for bax. In addition, R181H was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "R181H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10269", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant D259V was classified as recessive for RGC, p21, and PIG3, but it was classified as dominant negative for bax. In addition, D259V was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:08 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "D259V", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10270", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant E286K was classified as recessive for RGC, p21, and PIG3, but it was classified as dominant negative for bax. In addition, E286K was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:39 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "E286K", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10271", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant R283H was classified as recessive for p21 and PIG3, but it was classified as dominant negative for bax. In addition, R283H was classified as a hotspot for mutation (P < 0.01) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "R283H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10272", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant Y163N was classified as recessive for p21, but it was classified as dominant negative for bax and PIG3. In addition, Y163N was classified as a hotspot for mutation (P < 0.001) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "Y163N", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10273", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "A set of previously characterized p53 mutants was tested in the yeast assay to understand their transdominant potential (dominant negative). Each mutant was expressed equally with the wild-type p53. The authors used the RGC, p21, bax, and PIG3 sequences as p53 binding sites. TP53 variant L257P was classified as recessive for p21, but it was classified as dominant negative for RGC, bax and PIG3. In addition, L257P was classified as a hotspot for mutation (P < 0.014) by the authors. The authors proposed a hierarchy of dominance of p53 variants for p21, PIG3, and bax sequences. They observed p53 variants that are dominant negative for p21 are also dominant for PIG3 and bax, and p53 variants that are dominant negative for PIG3 are also dominant for bax. The authors suggested lack of transactivation ability is necessary but not sufficient to predict dominance.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 11896595 ], "rating": "2", "representative_transcript": null, "transcripts": null, "variant": "L257P", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10528", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant R156H originally identified in an oral lesion. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing p53 variant and WT p53 produced red/pink colonies, demonstrating that R156H displays transdominance. Authors reported that all of the DN mutants affected the amino acids essential to the upkeep of DNA binding surfaces according to crystallographic structure.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:14 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "R156H", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10529", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant H178P originally identified in glioblastoma. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing p53 variant and WT p53 produced red/pink colonies, demonstrating that H178P displays transdominance. Authors reported that all of the DN mutants affected the amino acids essential to the upkeep of DNA binding surfaces according to crystallographic structure.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:14 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "H178P", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10530", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant H179R originally identified in an oral lesion. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing p53 variant and WT p53 produced red/pink colonies, demonstrating that H179R displays transdominance. Authors reported that all of the DN mutants affected the amino acids essential to the upkeep of DNA binding surfaces according to crystallographic structure.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "H179R", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10531", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant R181P originally identified in breast cancer. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing p53 variant and WT p53 produced red/pink colonies, demonstrating that R181P displays transdominance. Authors reported that all of the DN mutants affected the amino acids essential to the upkeep of DNA binding surfaces according to crystallographic structure.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:08 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "R181P", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10540", "evidence_direction": "Supports", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant R249S. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing p53 variant and WT p53 produced red/pink colonies, demonstrating that R249S displays transdominance. Authors reported that all of the DN mutants affected the amino acids essential to the upkeep of DNA binding surfaces according to crystallographic structure.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:47 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "R249S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10554", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant L111R originally identified in anaplastic astrocytoma. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing L111R and WT p53 produced white colonies, indicating that L111R is not DN.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:14 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "L111R", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10555", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant H115Y originally identified in anaplastic astrocytoma from a glioma cell line. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing H115Y and WT p53 produced white colonies, indicating that H115Y is not DN.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:14 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "H115Y", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10556", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant C124R originally identified in anaplastic astrocytoma. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing C124R and WT p53 produced white colonies, indicating that C124R is not DN.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:14 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "C124R", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10558", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant L139N originally identified in breast cancer. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing L139N and WT p53 produced white colonies, indicating that L139N is not DN.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:14 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "L139N", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10574", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant G266V originally identified in breast cancer. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing G266V and WT p53 produced white colonies, indicating that G266V is not DN.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:14 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G266V", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10575", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant G266E originally identified in glioblastoma from a glioma cell line. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing G266E and WT p53 produced white colonies, indicating that G266E is not DN.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:47:12 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "G266E", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." }, { "asco_entry": null, "clinical_significance": "Dominant Negative", "disease": null, "doid": null, "drug_interaction_type": null, "drugs": null, "entrez_id": null, "evidence_civic_url": "https://civicdb.org/links/evidence_items/10576", "evidence_direction": "Does Not Support", "evidence_level": "D", "evidence_statement": "Yeast strain yIG397 was cultured to express both wild-type (WT) and mutant F270S originally identified in breast cancer. Should the mutant be dominant-negative (DN), TP53 will not bind and transactivate the ADE2 protein, resulting in red/pink colonies. If the mutant is recessive, then WT function is not blocked and ADE2 protein is expressed through TP53 transactivation, resulting in white colonies. Western blot analysis showed that yeast lysates showed expression of both WT and mutant alleles. Yeast expressing F270S and WT p53 produced white colonies, indicating that F270S is not DN.", "evidence_status": "accepted", "evidence_type": "Functional", "gene": "TP53", "gene_civic_url": null, "last_review_date": "2023-01-09 21:46:42 UTC", "nct_ids": null, "normalized_drug": null, "phenotypes": null, "pub_med_references": [ 10519380 ], "rating": "3", "representative_transcript": null, "transcripts": null, "variant": "F270S", "variant_civic_url": null, "variant_origin": "Somatic", "variant_summary": null, "gene_description": "TP53 mutations are universal across cancer types. The loss of a tumor suppressor is most often through large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide missense variants. These variants are broadly distributed throughout the gene, but with the majority localizing in the DNA binding domain. There is no single hotspot in the DNA binding domain, but a majority of mutations occur in amino acid positions 175, 245, 248, 273, and 282 (NM_000546) (Olivier et al., 2010). To fulfill its proper biological function four TP53 polypeptides must form a tetramer which functions as a transcription factor, therefore even if one out of four polypeptides has inactivating mutation it may lead to dominant negative phenotype of variable degree. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) variants have been found to have a prognostic impact on patient outcomes. The significance of many polymorphisms for susceptibility and prognosis of disease is still very much up for debate." } ] }, "dbnsfp_genes": { "version": "4.8", "items": [ { "kegg": { "id": [ "hsa04010", "hsa04110", "hsa04115", "hsa04210", "hsa04310", "hsa05030", "hsa05040", "hsa05210", "hsa05212", "hsa05213", "hsa05214", "hsa05215", "hsa05216", "hsa05217", "hsa05218", "hsa05219", "hsa05220", "hsa05222", "hsa05223" ], "full": [ "MAPK signaling pathway", "Cell cycle", "p53 signaling pathway", "Apoptosis", "Wnt signaling pathway", "Amyotrophic lateral sclerosis (ALS)", "Huntington's disease", "Colorectal cancer", "Pancreatic cancer", "Endometrial cancer", "Glioma", "Prostate cancer", "Thyroid cancer", "Basal cell carcinoma", "Melanoma", "Bladder cancer", "Chronic myeloid leukemia", "Small cell lung cancer", "Non-small cell lung cancer" ] }, "expressions_rpkm": null, "gene_symbol": "TP53", "p_hi": 1.0, "gdi": 15.33, "gdi_phred": 0.5512, "loftool_score": 0.0009650000000000004, "hipred": 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Acetylation", "Autodegradation of the E3 ubiquitin ligase COP1", "Stabilization of p53", "Transcriptional activation of cell cycle inhibitor p21", "Transcriptional activation of p53 responsive genes", "p53-Dependent G1 DNA Damage Response", "p53-Dependent G1/S DNA damage checkpoint", "G1/S DNA Damage Checkpoints", "G2/M DNA damage checkpoint", "Activation of NOXA and translocation to mitochondria", "Activation of PUMA and translocation to mitochondria", "Activation of BH3-only proteins", "G2/M Checkpoints", "Chaperonin-mediated protein folding", "Intrinsic Pathway for Apoptosis", "Cell Cycle Checkpoints", "Oncostatin_M", "Association of TriC/CCT with target proteins during biosynthesis", "Apoptosis", "Programmed Cell Death", "Hypoxic and oxygen homeostasis regulation of HIF-1-alpha", "Pre-NOTCH Transcription and Translation", "Pre-NOTCH Expression and Processing", "Signaling by NOTCH", "TP53 Regulates Metabolic Genes", "Aurora A signaling", "SUMOylation", "TP53 Regulates Transcription of Genes Involved in Cytochrome C Release", "cell cycle: g2/m checkpoint", "regulation of transcriptional activity by pml", "TP53 Regulates Transcription of Caspase Activators and Caspases", "Cellular responses to external stimuli", "TP53 regulates transcription of several additional cell death genes whose specific roles in p53-dependent apoptosis remain uncertain", "TP53 Regulates Transcription of Genes Involved in G1 Cell Cycle Arrest", "p53 signaling pathway", "TP53 Regulates Transcription of Genes Involved in G2 Cell Cycle Arrest", "atm signaling pathway", "TGF_beta_Receptor", "TP53 regulates transcription of additional cell cycle genes whose exact role in the p53 pathway remain uncertain", "TP53 Regulates Transcription of Cell Cycle Genes", "EGFR1", "TP53 Regulates Transcription of DNA Repair Genes", "Regulation of TP53 Expression", "Glucocorticoid receptor regulatory network", "Regulation of PTEN gene transcription", "The role of GTSE1 in G2/M progression after G2 checkpoint", "Hemostasis", "Ub-specific processing proteases", "rb tumor suppressor/checkpoint signaling in response to dna damage", "Regulation of TP53 Degradation", "Regulation of TP53 Expression and Degradation", "G2/M Transition", "Mitotic G2-G2/M phases", "PTEN Regulation", "PIP3 activates AKT signaling", "Ovarian tumor domain proteases", "Protein folding", "Deubiquitination", "Regulation of TP53 Activity through Phosphorylation", "Regulation of TP53 Activity through Association with Co-factors", "Regulation of TP53 Activity through Methylation", "Regulation of TP53 Activity through Acetylation", "Regulation of TP53 Activity", "Transcriptional Regulation by TP53", "Direct p53 effectors", "Cell Cycle", "Recruitment and ATM-mediated phosphorylation of repair and signaling proteins at DNA double strand breaks", "DNA Double Strand Break Response", "Cell Cycle, Mitotic", "Intracellular signaling by second messengers", "Signaling mediated by p38-alpha and p38-beta", "PLK3 signaling events", "Validated targets of C-MYC transcriptional activation", "AP-1 transcription factor network", "BARD1 signaling events", "p75(NTR)-mediated signaling", "Signaling events mediated by HDAC Class III", "p53 pathway", "LKB1 signaling events", "TP53 Regulates Transcription of Death Receptors and Ligands" ], "expression_gnf_atlas": [ "white blood cells", "superior cervical ganglion", "atrioventricular node", "placenta", "skeletal muscle" ], "expression_egenetics": [ "thymus", "epididymis", "tongue", "skin", "stomach", "testis", "lymphoreticular", "amniotic fluid", "larynx", "kidney", "uterus", "pancreas", "bile duct", "head and neck", "hypopharynx", "mammary gland", "skeletal muscle", "mesenchyma", "islets of Langerhans", "cervix", "vein", "spleen", "liver", "cartilage", "endometrium", "bone", "germinal center", "brain", "blood", "bone marrow", "lung", "ovary", "thyroid", "lymph node", "bladder", "frontal lobe", "colon", "placenta", "prostate", "breast" ], "pathway_uniprot": null, "function_description": "Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA- Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seems to have an effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1- mediated transcriptional activation of PER2 (PubMed:24051492). ", "disease_description": [ "TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma", "Esophageal cancer (ESCR) [MIM:133239]: A malignancy of the esophagus. The most common types are esophageal squamous cell carcinoma and adenocarcinoma. Cancer of the esophagus remains a devastating disease because it is usually not detected until it has progressed to an advanced incurable stage. The disease is caused by mutations affecting the gene represented in this entry", "Li-Fraumeni syndrome (LFS) [MIM:151623]: An autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers. ", "Squamous cell carcinoma of the head and neck (HNSCC) [MIM:275355]: A non-melanoma skin cancer affecting the head and neck. The hallmark of cutaneous SCC is malignant transformation of normal epidermal keratinocytes. The gene represented in this entry is involved in disease pathogenesis", "Lung cancer (LNCR) [MIM:211980]: A common malignancy affecting tissues of the lung. The most common form of lung cancer is non-small cell lung cancer (NSCLC) that can be divided into 3 major histologic subtypes: squamous cell carcinoma, adenocarcinoma, and large cell lung cancer. NSCLC is often diagnosed at an advanced stage and has a poor prognosis. The disease is caused by mutations affecting the gene represented in this entry", "Papilloma of choroid plexus (CPP) [MIM:260500]: A benign tumor of neuroectodermal origin that generally occurs in childhood, but has also been reported in adults. Although generally found within the ventricular system, choroid plexus papillomas can arise ectopically in the brain parenchyma or disseminate throughout the neuraxis. Patients present with signs and symptoms of increased intracranial pressure including headache, hydrocephalus, papilledema, nausea, vomiting, cranial nerve deficits, gait impairment, and seizures. ", "Adrenocortical carcinoma (ADCC) [MIM:202300]: A malignant neoplasm of the adrenal cortex and a rare childhood tumor. It occurs with increased frequency in patients with Beckwith- Wiedemann syndrome and Li-Fraumeni syndrome. ", "Basal cell carcinoma 7 (BCC7) [MIM:614740]: A common malignant skin neoplasm that typically appears on hair-bearing skin, most commonly on sun-exposed areas. It is slow growing and rarely metastasizes, but has potentialities for local invasion and destruction. It usually develops as a flat, firm, pale area that is small, raised, pink or red, translucent, shiny, and waxy, and the area may bleed following minor injury. Tumor size can vary from a few millimeters to several centimeters in diameter. " ], "gene_damage_prediction": { "primary_immunodeficiency": { "autosomalrecessive": "Medium", "autosomaldominant": "Medium", "all": "Medium" }, "mendelian": { "autosomalrecessive": "Medium", "autosomaldominant": "Medium", "all": "Medium" }, "cancer": { "recessive": "Medium", "dominant": "Medium", "all": "Medium" }, "all": "Medium" }, "mgi_mouse_gene": "Trp53", "mgi_mouse_phenotype": [ "behavior/neurological phenotype (the observable actions or reactions of mammalian organisms that are manifested through development and lifespan)", "liver/biliary system phenotype", "respiratory system phenotype", "embryo phenotype", "neoplasm", "pigmentation phenotype", "normal phenotype", "mortality/aging (the observable characteristics related to the ability of a mammalian organism to live and age that are manifested throughout development and life span)", "reproductive system phenotype", "hematopoietic system phenotype", "cardiovascular system phenotype (the observable morphological and physiological characteristics of the mammalian heart, blood vessels, or circulatory system that are manifested through development and lifespan)", "vision/eye phenotype", "limbs/digits/tail phenotype", "hearing/vestibular/ear phenotype", "nervous system phenotype (the observable morphological and physiological characteristics of the extensive, intricate network of electochemical structures in the body that is comprised of the brain, spinal cord, nerves, ganglia and parts of the receptor organs that are manifested through development and lifespan)", "digestive/alimentary phenotype", "renal/urinary system phenotype", "skeleton phenotype", "cellular phenotype", "immune system phenotype", "homeostasis/metabolism phenotype", "adipose tissue phenotype (the observable morphological and physiological characteristics of mammalian fat tissue that are manifested through development and lifespan)", "endocrine/exocrine gland phenotype", "integument phenotype (the observable morphological and physiological characteristics of the skin and its associated structures, such as the hair, nails, sweat glands, sebaceous glands and other secretory glands that are manifested through development and lifespan)", "growth/size/body region phenotype", "craniofacial phenotype", "muscle phenotype" ], "zfin_zebrafish_gene": "tp53", "zfin_zebrafish_structure": "nucleate erythrocyte", "zfin_zebrafish_phenotype_quality": "immature", "zfin_zebrafish_phenotype_tag": "abnormal" } ] }, "exac_genes": { "version": "18-Sep-2018", "items": [ { "prec": 0.08775030000000002, "pnull": 0.0000267186, "pli": 0.912223, "syn_z": -0.042240200000000006, "mis_z": 1.37892, "cnv_score": -0.19665500000000002, "segdups": 0, "flag": false } ] }, "publications": { "publications": [], "genes": [ { "publications": [ { "referenced_by": [ "VarSome AI" ], "pub_med_id": 38908277 }, { "referenced_by": [ "VarSome AI" ], "pub_med_id": 38907827 }, { "referenced_by": [ "VarSome AI" ], "pub_med_id": 38903727 }, { "referenced_by": [ 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