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).
Hassan Awada, MD, of the Taussig Cancer Institute, Cleveland Clinic Foundation, discusses the use of newer machine-learning techniques to help decipher a set of prognostic subgroups that could predict survival, thus potentially improving on traditional methods and moving acute myeloid leukemia into the era of personalized medicine (Abstract 34).
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).
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).
Jorge E. Cortes, MD, of the Georgia Cancer Center at Augusta University, reviews four important studies of treatment advances in chronic myeloid leukemia (CML): nilotinib vs dasatinib in newly diagnosed disease; final 5-year results from the BFORE trial on bosutinib vs imatinib for chronic phase (CP) CML; data from the OPTIC trial on ponatinib for CP-CML; and a novel class of mutated cancer-related genes associated with the Philadelphia translocation (Abstracts 45, 46, 48, 49).
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).
