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).
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]).
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).
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).
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).
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).
