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).
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).
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).
Farhad Ravandi, MD, of The University of Texas MD Anderson Cancer Center, offers his expert perspective on key treatment studies in acute myeloid leukemia on the use of gilteritinib, consolidation chemotherapy, venetoclax, cladribine, azacitidine, quizartinib, decitabine, and CPX-351 (Session 616 [Abstracts 24- 29]).
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).
