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).
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).
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).
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).
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).
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).
