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TP53 mutation, or deletion of the 17p arm that carries the gene, is the single most common change in cancer and carries a worse outlook almost everywhere. In chronic lymphocytic leukaemia it decides treatment: chemotherapy is avoided and venetoclax's first approval was for del(17p) disease.
TP53 status is read by sequencing (mutations in exons 4 to 10) and del(17p) by FISH; in endometrial and other cancers p53 immunohistochemistry (overexpression or complete absence) is the surrogate. Venetoclax (Venclexta) was first approved in 2016 for CLL with 17p deletion as detected by an FDA-approved test, the Vysis CLL FISH Probe Kit being the companion diagnostic; its CLL indications have since broadened to all patients, and guidelines (iwCLL, NCCN) keep TP53 status as the reason to prefer targeted agents over chemoimmunotherapy. In AML and MDS, TP53 mutation defines an adverse-risk group in ELN 2022 and the WHO and ICC 2022 classifications; in endometrial cancer p53-abnormal is one of the four molecular classes.
In plain words · TP53 is the 'guardian of the genome', broken in half of all cancers. Fixing it directly has so far defeated every attempt, so drugs exploit what its loss makes cancers depend on.
A TP53 mutation or 17p deletion usually means the cancer is harder to treat with chemotherapy. In chronic lymphocytic leukaemia it means your team will choose a BTK inhibitor or venetoclax-based treatment instead of chemoimmunotherapy. In leukaemia and womb cancer it places the disease in a higher-risk group that changes how intensively it is treated and followed.
Written only from the label or guideline text cited on this page. Not medical advice; your own report and the reading your team gives it come first.
A pathogenic TP53 mutation by sequencing, deletion of 17p13 by FISH (the Vysis CLL probe set), or an abnormal p53 immunohistochemistry pattern (strong diffuse nuclear overexpression, complete absence, or cytoplasmic staining) as a surrogate.
“TP53: Deletion chromosome 17p (17p-)”
FDA: List of FDA-Authorized Companion Diagnostic DevicesNo approval uses this readout as a threshold. It is defined by European LeukemiaNet 2022 recommendations for AML (Döhner et al., Blood 2022): TP53 mutation as adverse risk.
| Threshold | Drug | Cancer | Regulator | Source |
|---|---|---|---|---|
| 17p deletion by FISH (historic first indication; the CLL indication is now unrestricted)historic The 2016 accelerated approval was for CLL with 17p deletion after at least one prior therapy; the current Venclexta label covers CLL and SLL without a TP53 restriction. | Venetoclax | Chronic lymphocytic leukaemia | FDA | label |
| Device | Maker | Indication and sample | Drug | PMA / 510(k) |
|---|---|---|---|---|
| Vysis CLL FISH Probe Kit | Abbott Molecular | B-cell Chronic Lymphocytic Leukemia - Peripheral Blood | Venetoclax | P150041 (04/11/2016) |
Matched on the name and aliases of the readout in the title, setting and summary of each trial; a match is a mention, not proof the readout was an entry criterion.
Shares Non-Hodgkin lymphoma (all types) and the tag biomarker.
Shares Richter transformation of chronic lymphocytic leukaemia, FISH / ISH (in situ hybridisation), Diffuse large B-cell lymphoma, Non-Hodgkin lymphoma (all types) and the tag biomarker.
Shares FISH / ISH (in situ hybridisation), Venetoclax, Diffuse large B-cell lymphoma, Non-Hodgkin lymphoma (all types) and the tag biomarker.
Shares Mantle cell lymphoma, Chronic lymphocytic leukaemia, Diffuse large B-cell lymphoma, Non-Hodgkin lymphoma (all types) and the tag biomarker.
Shares Richter transformation of chronic lymphocytic leukaemia, Diffuse large B-cell lymphoma, Non-Hodgkin lymphoma (all types) and the tag biomarker.
Shares IDH1 R132 mutation, Acute myeloid leukaemia and the tag biomarker.
Shares IDH1 R132 mutation, Acute myeloid leukaemia and the tag biomarker.
Shares FISH / ISH (in situ hybridisation), Non-Hodgkin lymphoma (all types) and the tag biomarker.