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).
Hassan Awada, MD, of the Taussig Cancer Institute, Cleveland Clinic Foundation, discusses the use of newer machine-learning techniques to help decipher a set of prognostic subgroups that could predict survival, thus potentially improving on traditional methods and moving acute myeloid leukemia into the era of personalized medicine (Abstract 34).
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).
Corey Cutler, MD, MPH, of Dana-Farber Cancer Institute, discusses results from a multicenter trial that compared reduced-intensity allogeneic hematopoietic cell transplantation to hypomethylating therapy or best supportive care in patients aged 50 to 75 with advanced myelodysplastic syndromes (Abstract 75).
Curtis Lachowiez, MD, of The University of Texas MD Anderson Cancer Center, discusses an interim analysis of a phase Ib/II study showing that venetoclax plus chemotherapy represents an effective regimen, particularly in patients with newly diagnosed and relapsed or refractory acute myeloid leukemia. The regimen appears to be an effective bridge to hematopoietic stem cell transplantation (Abstract 332).
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).
