Farhad Ravandi, MD, of The University of Texas MD Anderson Cancer Center, offers his expert perspective on key treatment studies in acute myeloid leukemia on the use of gilteritinib, consolidation chemotherapy, venetoclax, cladribine, azacitidine, quizartinib, decitabine, and CPX-351 (Session 616 [Abstracts 24- 29]).
Lena E. Winestone, MD, MSHP, of the University of California, San Francisco and Benioff Children’s Hospital, reviews different aspects of bias in treatment delivery, including patient selection for clinical trials; racial and ethnic disparities in survival for indolent non-Hodgkin diffuse large B-cell lymphomas; and end-of-life hospitalization of patients with multiple myeloma, as well as outcome disparities (Abstracts 207-212).
Emmanuel Bachy, MD, PhD, of the Hospices Civils de Lyon, discusses the final analysis of a phase III study of adding romidepsin to chemotherapy in patients with previously untreated peripheral T-cell lymphoma. Adding romidepsin did not improve progression-free survival and was associated with high rates of adverse events (Abstract 39).
Tycel J. Phillips, MD, of the University of Michigan Rogel Cancer Center, discusses phase II data from the CITADEL-204 study, showing that patients with relapsed or refractory marginal zone lymphoma who were not previously treated with a Bruton’s tyrosine kinase inhibitor achieved rapid and durable responses with single-agent parsaclisib. Comparable results were also observed in patients with nodal, extranodal, or splenic disease (Abstract 338).
Smita Bhatia, MD, MPH, and Radhika Gangaraju, MD, both of the Institute for Cancer Outcomes and Survivorship, University of Alabama at Birmingham, discuss findings that showed survivors of bone marrow transplants are at a 7- to 12-fold higher risk of coronary heart disease than a sibling comparison group. They recommend aggressive management of cardiovascular risk factors to prevent morbidity from heart disease in this patient population (Abstract 73).
Ari M. Melnick, MD, of Weill Cornell Medicine, discusses the BCL10 mutation in patients with activated B-cell–like diffuse large B-cell lymphoma, and his study results which showed that the mutation should be considered as a biomarker for ibrutinib resistance so that alternative targeted treatments can be prioritized (Abstract 3).
