Musa Yilmaz, MD, of The University of Texas MD Anderson Cancer Center, discusses study results suggesting that quizartinib with decitabine and venetoclax is active in patients with FLT3-ITD–mutated acute myeloid leukemia and that RAS/MAPK mutations continue to drive primary and secondary resistance (Abstract 370).
Anil Aktas-Samur, PhD, of Dana-Farber Cancer Institute, discusses study findings on the genomic characterization of non-progressor smoldering multiple myeloma, results that may provide a molecular definition of the disease as well as its risk-driving features. Combining this low-risk model with current high-risk models may possibly improve clinical trials for patients with this early precursor to myeloma (Abstract 545).
Michael R. Bishop, MD, of the University of Chicago, discusses insights from findings of the phase III BELINDA study, which may inform the design of future CAR T-cell trials, as well as the use of second-line tisagenlecleucel therapy in patients with relapsed or refractory aggressive B-cell non-Hodgkin lymphoma (Abstract LBA-6).
Sangeetha Venugopal, MD, of The University of Texas MD Anderson Cancer Center, discusses a retrospective analysis of 562 patients with treated secondary acute myeloid leukemia and prior exposure to hypomethylating agents (HMAs). The results showed that an HMA plus venetoclax yielded significantly higher overall response rates and improved overall survival compared with intensive chemotherapy or low-intensity chemotherapy, particularly in patients 60 years or older who had a karyotype without adverse risk (Abstract 794).
Talha Badar, MD, of the Mayo Clinic, discusses the near-universal poor outcomes for patients with TP53-mutated acute myeloid leukemia and the findings that show allogeneic stem cell transplantation appears to improve the long-term survival in a subset of these patients. Effective therapies may successfully bridge patients to transplant and prolong survival for those who are transplant-ineligible (Abstract 797).
Masayuki Umeda, MD, of St. Jude Children's Research Hospital, discusses his research which showed that UBTF-TD (upstream binding transcription factor-tandem duplications) define a unique subtype of acute myeloid leukemia that previously lacked a clear oncogenic driver. UBTF-TD is associated with FLT3-ITD and WT1 mutations, adolescent age, and poor outcomes. These alterations are critical for future risk-stratification for this patient cohort.
