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).
Manali Kamdar, MD, of the University of Colorado Cancer Center, discusses phase III results from the TRANSFORM study, which suggest that lisocabtagene maraleucel, a CD19-directed CAR T-cell therapy, improved outcomes with a favorable safety profile and may be a potential new standard of care for second-line treatment of patients with relapsed or refractory large B-cell lymphoma (Abstract 91).
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).
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).
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).
Roni Shouval, MD, PhD, of Memorial Sloan Kettering Cancer Center, discusses his findings, which show, for the first time, that TP53 alterations are a valuable prognostic and potentially predictive marker in patients with large B-cell lymphoma who receive CD19–CAR T-cell therapy. Gene-expression profiling suggests that TP53 alterations result in an immunosuppressive tumor microenvironment and impaired apoptosis signaling, which could lead to decreased CAR T-cell therapy efficacy (Abstract 710).
