Jyoti Nangalia, MBBChir, of Wellcome Sanger Institute and the University of Cambridge, discusses how her team used large-scale whole-genome sequencing to precisely time the origins of a blood cancer and measure how it grew. The information could provide opportunities for early diagnosis and intervention (Abstract LBA-1).
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).
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).
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).
Lena E. Winestone, MD, MSHP, of the University of California, San Francisco and Benioff Children’s Hospital, reviews different aspects of bias in treatment delivery, including patient selection for clinical trials; racial and ethnic disparities in survival for indolent non-Hodgkin diffuse large B-cell lymphomas; and end-of-life hospitalization of patients with multiple myeloma, as well as outcome disparities (Abstracts 207-212).
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]).
