Ann-Kathrin Eisfeld, MD, of The Ohio State University Comprehensive Cancer Center, discusses SEER data showing that patients with acute myeloid leukemia who are Black and younger than age 60 may have poor survival outcomes, a disparity that should be addressed and further studied to establish molecular risk profiles (Abstract 6).
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]).
Matthew S. Davids, MD, of Dana-Farber Cancer Institute, summarizes three key studies from a session he co-moderated on ibrutinib plus venetoclax for first-line treatment of patients with chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL), long-term responses to these agents for relapsed and refractory CLL, and undetectable minimal residual disease following fixed-duration treatment with venetoclax and rituximab for CLL (Abstracts 123, 124, and 125).
Sara Zarnegar-Lumley, MD, of Vanderbilt University Medical Center, discusses an analysis of a large cohort confirming the age-associated prevalence of IDH mutations in patients, across the age spectrum, with acute myeloid leukemia and therapeutic implications. IDH-mutated genes were found to co-occur frequently with other mutations, some of which favorably impact outcomes in patients younger than 60 (Abstract 388).
Jyoti Nangalia, MBBChir, of Wellcome Sanger Institute and the University of Cambridge, discusses how her team used large-scale whole-genome sequencing to precisely time the origins of a blood cancer and measure how it grew. The information could provide opportunities for early diagnosis and intervention (Abstract LBA-1).
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).
