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).
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).
Hassan Awada, MD, of the Taussig Cancer Institute, Cleveland Clinic Foundation, discusses the use of newer machine-learning techniques to help decipher a set of prognostic subgroups that could predict survival, thus potentially improving on traditional methods and moving acute myeloid leukemia into the era of personalized medicine (Abstract 34).
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).
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).
