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).
Eunice S. Wang, MD, of Roswell Park Comprehensive Cancer Center, discusses phase III results showing that gilteritinib and azacitidine led to significantly higher composite complete response rates in patients with newly diagnosed FLT3-mutant acute myeloid leukemia who are ineligible for intensive induction chemotherapy. Overall survival was similar to that of azacitidine alone (Abstract 700).
Joe Schroers-Martin, MD, of Stanford University, discusses his latest study findings, which show that follicular lymphoma driver mutations are detectable in blood and saliva years prior to a clinical diagnosis. These data build on previous work and suggest that researchers may be able to stratify people at elevated risk of clinical malignancy (Abstract 709).
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).
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).
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.
