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).
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).
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).
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).
Tycel J. Phillips, MD, of the University of Michigan Rogel Cancer Center, discusses phase II data from the CITADEL-204 study, showing that patients with relapsed or refractory marginal zone lymphoma who were not previously treated with a Bruton’s tyrosine kinase inhibitor achieved rapid and durable responses with single-agent parsaclisib. Comparable results were also observed in patients with nodal, extranodal, or splenic disease (Abstract 338).
