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).
Corey Cutler, MD, MPH, of Dana-Farber Cancer Institute, discusses results from a multicenter trial that compared reduced-intensity allogeneic hematopoietic cell transplantation to hypomethylating therapy or best supportive care in patients aged 50 to 75 with advanced myelodysplastic syndromes (Abstract 75).
Ann-Kathrin Eisfeld, MD, of The Ohio State University Comprehensive Cancer Center, discusses SEER data showing that patients with acute myeloid leukemia who are Black and younger than age 60 may have poor survival outcomes, a disparity that should be addressed and further studied to establish molecular risk profiles (Abstract 6).
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).
Paul G. Richardson, MD, of Dana-Farber Cancer Institute, gives his expert perspective on three important studies in multiple myeloma: long-term results from the IFM 2009 trial on early vs late autologous stem cell transplant in patients with newly diagnosed disease; the effect of high-dose melphalan on mutational burden in relapsed disease; and daratumumab plus lenalidomide, bortezomib, and dexamethasone in transplant-eligible patients with newly diagnosed disease (Abstracts 143, 61, and 549).
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).
