Mark Bustoros, MD, on Ixazomib/Lenalidomide/Dexamethasone for High-Risk Smoldering Multiple Myeloma
2019 ASH Annual Meeting & Exposition
Mark Bustoros, MD, of Dana-Farber Cancer Institute, discusses phase II study results showing that the combination of ixazomib, lenalidomide, and dexamethasone is effective in patients with high-risk smoldering disease, with a high response rate, convenient schedule, and manageable toxicity. Longer follow-up for disease outcome is ongoing (Abstract 580).
Mikkael A. Sekeres, MD, of the Cleveland Clinic, discusses results of a phase Ib study of glasdegib in combination with azacitidine, which showed activity in patients with untreated myelodysplastic syndromes, acute myeloid leukemia, and chronic myelomonocytic leukemia who are ineligible for intensive chemotherapy (Abstract 177).
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).
Ilaria Iacobucci, PhD, of St. Jude Children’s Research Hospital, discusses her work to more accurately define mutation subtypes in acute myeloid leukemia and myelodysplastic syndromes, as well as the implications for diagnosis, prognosis, and treatment (Abstract LBA-4 ).
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).
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).
