Deletion 17p Subclones and Outcomes in Patients With CLL
Posted: Thursday, May 20, 2021
According to findings presented in the British Journal of Haematology, low-frequency deletions of 17p subclones may not necessarily be associated with worse outcomes for elderly, treatment-naive patients with chronic lymphocytic leukemia (CLL) treated with fludarabine, cyclophosphamide, and rituximab (FCR). Bryone Kuss, PhD, of Flinders University, Adelaide, Australia, and colleagues also identified a “significant” co-occurrence of deletion 13q proteins in CLL cases with low-frequency 17p clones, demonstrating that these abnormalities may not always occur within the same cell.
“These findings highlight the clonal heterogeneity of CLL and challenge the notion that acquisition of del17p is a late-driver event in leukemogenesis, as our present data demonstrate that in some cases this lesion may precede or occur in parallel with del13q,” the authors added.
In this study, the authors analyzed pretreatment peripheral blood samples from 95 patients in the Australasian Leukaemia and Lymphoma Group (ALLG) CLL5 clinical trial, which examined the safety, tolerability, and efficacy of an FCR regimen in elderly, treatment-naive patients with CLL. The authors used slide-based fluorescence in situ hybridization to identify deletions of 11q, 17p, trisomy 12, and 13q.
In 20 of the 95 patients, the authors identified deletion of 17p. Among those patients, 15 had low-frequency subclones of deletion 17 (16%). Subclones solely with deletion 17p or deletion 13q were also noted in 11 of those 15 patients.
Patients with low-frequency deletion 17p, without TP53 mutations, were reported to have longer median progression-free survival (48.6 months) and overall survival (48.6 months) than patients high-frequency deletion 17p clones (14.3 months and 28.4 months, respectively). Patients without deletion 17p subclones had a progression-free survival of 55.5 months and an overall survival of 77.8 months.
Disclosure: For full disclosure of the study authors, visit wiley.com.
