Edward A. Stadtmauer, MD, on Advanced Multiple Myeloma and Sarcoma: First-in-Human Assessment of CRISPR-Edited T Cells
2019 ASH Annual Meeting & Exposition
Edward A. Stadtmauer, MD, of the University of Pennsylvania Abramson Cancer Center, discusses phase I results of immune cells, modified with CRISPR/Cas9 technology, and infused in three patients (two with multiple myeloma and one with sarcoma). Researchers observed the cells expand and bind to their tumor targets with no serious side effects (Abstract 49).
Andrew H. Wei, MBBS, PhD, of The Alfred Hospital, Melbourne, discusses phase III findings on oral azacitidine (CC-486), the first treatment used in the maintenance setting shown to improve both overall and disease-free survival in patients with acute myeloid leukemia that is in remission following induction chemotherapy (Abstract LBA-3).
C. Ola Landgren, MD, PhD, of Memorial Sloan Kettering Cancer Center, discusses phase II study findings that showed an 83% negative rate of minimal residual disease in newly diagnosed multiple myeloma treated weekly with 8 cycles of the quadruplet regimen of carfilzomib/lenalidomide/dexamethasone/daratumumab, without autologous stem cell transplant (Abstract 862).
David P. Steensma, MD, of Dana-Farber Cancer Institute, discusses early study findings on H3B-8800, which decreased the need for red blood cell or platelet transfusion in 14% of patients. This splicing modulator, used in the trial to treat patients with hematologic malignancies, also showed safety, dose-dependent target engagement, and a predictable pharmacokinetic profile (Abstract 673).
Tait D. Shanafelt, MD, of Stanford University, discusses extended follow-up data that show ibrutinib plus rituximab improved clinical outcomes vs the standard therapy of fludarabine/cyclophosphamide/ rituximab in younger patients with previously untreated chronic lymphocytic leukemia (Abstract 33).
Jerald P. Radich, MD, of the Fred Hutchinson Cancer Research Center, discusses a gene-expression model that distinguishes patients with chronic myeloid leukemia who achieved a deep molecular response from those with a poor response to treatment. This work could yield new therapeutic targets that could potentially turn a poor responder into a good responder who might even achieve treatment-free remission (Abstract 665).
