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).
Andrew D. Zelenetz, MD, PhD, of Memorial Sloan Kettering Cancer Center, offers his expert views on five treatment studies in mantle cell lymphoma focusing on the next-generation BTK inhibitor LOXO-305; lisocabtagene maraleucel; minimal residual disease monitoring following autologous stem cell transplantation with or without rituximab maintenance; the antibody-drug conjugate VLS-101; and venetoclax, lenalidomide, and rituximab (Abstracts 117, 118, 120, 121, 122).
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).
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).
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).
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).
