Christian Marinaccio, PhD Candidate: Genetic Driver May Play a Role in Progression of Myeloproliferative Neoplasms to AML
2020 ASH Annual Meeting & Exposition
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).
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).
Steven M. Horwitz, MD, of Memorial Sloan Kettering Cancer Center, discusses phase II data from the Primo trial, which support continued evaluation of duvelisib as a treatment option for relapsed or refractory peripheral T-cell lymphoma due to consistent response rates (Abstract 44).
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]).
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).