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).
Steven M. Horwitz, MD, of Memorial Sloan Kettering Cancer Center, discusses data from the largest multicenter retrospective analysis of allogeneic hematopoietic transplantation, which supports its curative potential in patients with mature T-cell lymphoma, a group marked by poor survival and limited treatment options (Abstract 41).
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).
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).
David T. Teachey, MD, of the University of Pennsylvania and Children’s Hospital of Philadelphia, discusses data showing that cranial radiation might be eliminated in most children with T-cell acute lymphoblastic leukemia and that bortezomib may improve survival in children with T-cell lymphoblastic lymphoma (Abstract 266).
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).
