Eunice S. Wang, MD, on FLT3-Mutated AML: Gilteritinib and Azacitidine for Intensive Induction Chemotherapy–Ineligible Patients
2021 ASH Annual Meeting & Exposition
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).
The ASCO Post Staff
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.
The ASCO Post Staff
Matthew S. Davids, MD, of Dana-Farber Cancer Institute, discusses phase II results from a multicenter study that showed the efficacy of ibrutinib plus fludarabine, cyclophosphamide, and rituximab in younger, fit patients with chronic lymphocytic leukemia who desire the possibility of a functional cure with time-limited therapy (Abstract 640).
The ASCO Post Staff
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).
The ASCO Post Staff
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).
The ASCO Post Staff
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).
