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).
Matthew S. Davids, MD, of Dana-Farber Cancer Institute, discusses phase II results from a multicenter study that showed the efficacy of ibrutinib plus fludarabine, cyclophosphamide, and rituximab in younger, fit patients with chronic lymphocytic leukemia who desire the possibility of a functional cure with time-limited therapy (Abstract 640).
Michael R. Bishop, MD, of the University of Chicago, discusses insights from findings of the phase III BELINDA study, which may inform the design of future CAR T-cell trials, as well as the use of second-line tisagenlecleucel therapy in patients with relapsed or refractory aggressive B-cell non-Hodgkin lymphoma (Abstract LBA-6).
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).
Nikhil C. Munshi, MD, PhD, of Dana-Farber Cancer Institute, discusses the findings from a large nationwide Veterans Affairs study, which showed that, for patients with multiple myeloma, the effectiveness of the COVID-19 vaccine is reduced, likely due to patients’ immunosuppression. Dr. Munshi describes what next steps should be taken (Abstract 400).
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).
