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).
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).
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).
Nitin Jain, MD, of The University of Texas MD Anderson Cancer Center, reviews six important abstracts on CAR T-cell treatments for B-cell acute lymphoblastic leukemia (ALL): successful 24-hour manufacture of CAR T-cell therapy; ALLCAR19, a novel fast-off rate therapy; donor-derived CD19-targeted treatment; CAR 2.0 therapy to manage post-transplant relapse; UCART22, allogeneic engineered T cells expressing anti-CD22 chimeric antigen receptor; and inotuzumab ozogamicin in pediatric CD-22–positive disease (Session 614, Abstracts 159-164).
Christian Marinaccio, PhD Candidate, of Northwestern University, describes research he is conducting in the laboratory of John D. Crispino, PhD, which shows the loss of the tumor suppressor gene LKB1/STK11 facilitates progression of myeloproliferative neoplasms to acute myeloid leukemia (Abstract 1).
