C. Ola Landgren, MD, PhD, on Carfilzomib, Lenalidomide, Dexamethasone, and Daratumumab for Newly Diagnosed Multiple Myeloma
2019 ASH Annual Meeting & Exposition
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).
Patrick A. Brown, MD, of Johns Hopkins University, discusses phase III findings from a Children’s Oncology Group Study showing that blinatumomab was superior to chemotherapy in terms of efficacy and tolerability for young patients as a post-reinduction therapy in the setting of high- and intermediate-risk first relapse of B-cell acute lymphoblastic leukemia (Abstract LBA-1).
Nitin Jain, MD, of The University of Texas MD Anderson Cancer Center, discusses findings from two studies showing that the combination of ibrutinib and venetoclax is an effective chemotherapy-free oral regimen for patients with high-risk, previously untreated chronic lymphocytic leukemia (Abstract 34).
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).
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).
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).
