Meletios A. Dimopoulos, MD, of the University of Athens, discusses data from the phase III APOLLO study, which evaluated the use of subcutaneous daratumumab plus pomalidomide and dexamethasone, vs pomalidomide and dexamethasone alone, in patients with relapsed or refractory multiple myeloma (Abstract 412).
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).
Smita Bhatia, MD, MPH, and Radhika Gangaraju, MD, both of the Institute for Cancer Outcomes and Survivorship, University of Alabama at Birmingham, discuss findings that showed survivors of bone marrow transplants are at a 7- to 12-fold higher risk of coronary heart disease than a sibling comparison group. They recommend aggressive management of cardiovascular risk factors to prevent morbidity from heart disease in this patient population (Abstract 73).
Emmanuel Bachy, MD, PhD, of the Hospices Civils de Lyon, discusses the final analysis of a phase III study of adding romidepsin to chemotherapy in patients with previously untreated peripheral T-cell lymphoma. Adding romidepsin did not improve progression-free survival and was associated with high rates of adverse events (Abstract 39).
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).
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).
