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).
Alba Rodriguez-Meira, DPhil, of the University of Oxford, discusses a comprehensive analysis of the genetic, cellular, and molecular landscape of TP53-mediated transformation, providing insights into the evolution of chronic hematologic malignancies toward an aggressive acute leukemia. Because TP53 is the most commonly mutated gene in human cancer, these findings may well be of broad relevance (Abstract 3).
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).
Andrew Matthews, MD, of the Abramson Cancer Center, University of Pennsylvania, discusses findings from a retrospective study at an academic institution, which showed there was no statistically significant difference in overall survival between induction with CPX-351 and venetoclax/azacitidine for adults with acute myeloid leukemia. Prospective studies to confirm similar effectiveness with careful attention to side effects, quality of life, and impact on transplant outcomes may help clinicians decide between these therapies (Abstract 795).
Carsten Utoft Niemann, MD, PhD, of Copenhagen University Hospital, discusses a primary analysis of the phase II Vision HO141 trial, which showed the feasibility of stopping and restarting ibrutinib and venetoclax in patients with relapsed or refractory chronic lymphocytic leukemia who have undetectable measurable residual disease. A favorable benefit-risk profile was demonstrated, with no new safety signals (Abstract 69).
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.
