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).
David T. Teachey, MD, of the University of Pennsylvania and Children’s Hospital of Philadelphia, discusses data showing that cranial radiation might be eliminated in most children with T-cell acute lymphoblastic leukemia and that bortezomib may improve survival in children with T-cell lymphoblastic lymphoma (Abstract 266).
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).
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).
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).
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).
