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]).
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).
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).
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).
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).
