A 65-year-old man with chronic lymphocytic leukaemia (CLL) is found to have del(17p13) on FISH. This deletion targets TP53 and predicts all of the following EXCEPT:
- A Resistance to fludarabine-based chemoimmunotherapy
- B Shortened overall survival compared to CLL without del(17p)
- C Poor response to ibrutinib (BTK inhibitor) ✓
- D Requirement for upfront targeted therapy rather than watch-and-wait for asymptomatic patients
Explanation
Del(17p13)/TP53 deletion in CLL renders it highly resistant to conventional chemotherapy (fludarabine, bendamustine, chlorambucil) because DNA-damaging drugs require intact p53 to trigger apoptosis. Overall survival is markedly shortened compared to IGHV-mutated CLL without this deletion. However, ibrutinib (BTK inhibitor) and venetoclax (BCL-2 inhibitor) act via p53-independent pathways and retain efficacy in del(17p) CLL — these are now the preferred agents. Asymptomatic patients with del(17p) are typically observed until they require treatment; the deletion itself (without symptoms/organomegaly/cytopenias) does not mandate upfront therapy.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.