Leukemia
Superior outcomes were observed for older patients with AML receiving decitabine + venetoclax for 10 days versus intensive chemotherapy in a propensity score–matched analysis, particularly for those at high risk for treatment-related mortality.
The addition of venetoclax to azacitidine in treatment-naïve patients with AML ineligible for intensive therapy because of medical comorbidities and/or advanced age (≥75 years) produced significantly greater response rates and overall survival versus azacitidine alone.
Ivosidenib monotherapy demonstrated prolonged overall survival and the potential to increase complete response rates in relapsed or refractory IDH1-mutated acute myeloid leukemia (AML) compared with standard-of-care therapies in a historical control population.
The QUAZAR study evaluating CC-486 (oral azacitidine) illustrated that CC-486 does not negatively impact health-related quality of life compared with placebo.
This study in younger and older patients with newly diagnosed, FLT3-mutated acute myeloid leukemia (AML) showed that midostaurin + chemotherapy resulted in high response rates, regardless of patient age.
The combination of enasidenib and azacitidine resulted in a significant increase in response rate when compared with azacitidine alone in patients with mutant IDH2 newly diagnosed AML. This combination therapy was well-tolerated.
Patient-specific doses of iodine-131-apamistamab resulted in consistent engraftment following allogeneic hematopoietic stem-cell transplantation among patients with relapsed/refractory (R/R) acute myeloid leukemia (AML).
Patients with FLT3 mutation–positive R/R AML who relapsed on gilteritinib therapy were found to have acquired new mutations that were not present at baseline. The most common mutations occurred in RAS/MAPK pathway genes and FLT3.Patients with mutations in RAS/MAPK pathway genes at baseline still benefited from gilteritinib therapy.
Selinexor in combination with standard induction and consolidation therapy appears highly active in older patients with de novo acute myeloid leukemia.
This first-in-human study indicates that CLL1-CD33 cCAR has favorable efficacy and manageable toxicity in patients with R/R AML.
