In CLL, deletion of 17p13 (TP53 loss) is clinically important because it predicts:
- A Richter transformation to DLBCL
- B Excellent response to fludarabine-cyclophosphamide-rituximab (FCR)
- C Resistance to alkylating agents and purine analogues; Ibrutinib preferred ✓
- D Autoimmune hemolytic anemia as the dominant complication
Explanation
del17p/TP53 mutation confers resistance to DNA-damaging agents (fludarabine, cyclophosphamide, bendamustine) because functional p53 is required for apoptosis induction by these drugs. Current guidelines mandate BTK inhibitors (ibrutinib, acalabrutinib) or venetoclax ± obinutuzumab as first-line therapy for this high-risk group. FCR achieves high response rates only in IGHV-mutated del13q cases. Richter transformation is associated with IGHV-unmutated, complex karyotype disease but not specifically del17p. AIHA is a complication of CLL but not driven by del17p.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.