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).
Nitin Jain, MD, of The University of Texas MD Anderson Cancer Center, reviews six important abstracts on CAR T-cell treatments for B-cell acute lymphoblastic leukemia (ALL): successful 24-hour manufacture of CAR T-cell therapy; ALLCAR19, a novel fast-off rate therapy; donor-derived CD19-targeted treatment; CAR 2.0 therapy to manage post-transplant relapse; UCART22, allogeneic engineered T cells expressing anti-CD22 chimeric antigen receptor; and inotuzumab ozogamicin in pediatric CD-22–positive disease (Session 614, Abstracts 159-164).
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).
Caron A. Jacobson, MD, of the Dana-Farber Cancer Institute, discusses results from the ZUMA-9 C2 study, an ongoing trial that is exploring axicabtagene ciloleucel in patients with relapsed or refractory large B-cell lymphoma (Abstract 2100).
Emmanuel Bachy, MD, PhD, of the Hospices Civils de Lyon, discusses the final analysis of a phase III study of adding romidepsin to chemotherapy in patients with previously untreated peripheral T-cell lymphoma. Adding romidepsin did not improve progression-free survival and was associated with high rates of adverse events (Abstract 39).
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).
