Paolo Ghia, MD, PhD, on CLL: New Data on Treatment With Ibrutinib Plus Venetoclax
2021 ASH Annual Meeting & Exposition
Paolo Ghia, MD, PhD, of the Università Vita-Salute San Raffaele and IRCCS Ospedale San Raffaele, discusses disease-free survival results from the measurable residual disease cohort of the phase II CAPTIVATE trial. This multicenter trial focuses on first-line ibrutinib plus venetoclax in patients with chronic lymphocytic leukemia (Abstract 68).
The ASCO Post Staff
Carsten Utoft Niemann, MD, PhD, of Copenhagen University Hospital, discusses a primary analysis of the phase II Vision HO141 trial, which showed the feasibility of stopping and restarting ibrutinib and venetoclax in patients with relapsed or refractory chronic lymphocytic leukemia who have undetectable measurable residual disease. A favorable benefit-risk profile was demonstrated, with no new safety signals (Abstract 69).
The ASCO Post Staff
Masayuki Umeda, MD, of St. Jude Children's Research Hospital, discusses his research which showed that UBTF-TD (upstream binding transcription factor-tandem duplications) define a unique subtype of acute myeloid leukemia that previously lacked a clear oncogenic driver. UBTF-TD is associated with FLT3-ITD and WT1 mutations, adolescent age, and poor outcomes. These alterations are critical for future risk-stratification for this patient cohort.
The ASCO Post Staff
Joe Schroers-Martin, MD, of Stanford University, discusses his latest study findings, which show that follicular lymphoma driver mutations are detectable in blood and saliva years prior to a clinical diagnosis. These data build on previous work and suggest that researchers may be able to stratify people at elevated risk of clinical malignancy (Abstract 709).
The ASCO Post Staff
Roni Shouval, MD, PhD, of Memorial Sloan Kettering Cancer Center, discusses his findings, which show, for the first time, that TP53 alterations are a valuable prognostic and potentially predictive marker in patients with large B-cell lymphoma who receive CD19–CAR T-cell therapy. Gene-expression profiling suggests that TP53 alterations result in an immunosuppressive tumor microenvironment and impaired apoptosis signaling, which could lead to decreased CAR T-cell therapy efficacy (Abstract 710).
The ASCO Post Staff
Musa Yilmaz, MD, of The University of Texas MD Anderson Cancer Center, discusses study results suggesting that quizartinib with decitabine and venetoclax is active in patients with FLT3-ITD–mutated acute myeloid leukemia and that RAS/MAPK mutations continue to drive primary and secondary resistance (Abstract 370).
