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).
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).
Tycel Phillips, MD, of the Rogel Cancer Center, University of Michigan, discusses phase II findings from the CITADEL-204 study of parsaclisib, a next-generation inhibitor of phosphatidylinositol 3-kinase. The agent, used as a monotherapy, appeared to benefit patients with relapsed or refractory marginal zone lymphoma who had a rapid and durable clinical response (Abstract 44).
Manali Kamdar, MD, of the University of Colorado Cancer Center, discusses phase III results from the TRANSFORM study, which suggest that lisocabtagene maraleucel, a CD19-directed CAR T-cell therapy, improved outcomes with a favorable safety profile and may be a potential new standard of care for second-line treatment of patients with relapsed or refractory large B-cell lymphoma (Abstract 91).
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).
Alba Rodriguez-Meira, DPhil, of the University of Oxford, discusses a comprehensive analysis of the genetic, cellular, and molecular landscape of TP53-mediated transformation, providing insights into the evolution of chronic hematologic malignancies toward an aggressive acute leukemia. Because TP53 is the most commonly mutated gene in human cancer, these findings may well be of broad relevance (Abstract 3).
