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).
Paul G. Richardson, MD, of Dana-Farber Cancer Institute, gives his expert perspective on three important studies in multiple myeloma: long-term results from the IFM 2009 trial on early vs late autologous stem cell transplant in patients with newly diagnosed disease; the effect of high-dose melphalan on mutational burden in relapsed disease; and daratumumab plus lenalidomide, bortezomib, and dexamethasone in transplant-eligible patients with newly diagnosed disease (Abstracts 143, 61, and 549).
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).
Meletios A. Dimopoulos, MD, of the University of Athens, discusses data from the phase III APOLLO study, which evaluated the use of subcutaneous daratumumab plus pomalidomide and dexamethasone, vs pomalidomide and dexamethasone alone, in patients with relapsed or refractory multiple myeloma (Abstract 412).
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).
