1. Cardiotoxicity of CPX-351 in children and adolescents with relapsed AML: a Children's Oncology Group report
- Author
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Kasey J. Leger, Michael J. Absalon, Biniyam G. Demissei, Amanda M. Smith, Robert B. Gerbing, Todd A. Alonzo, Hari K. Narayan, Betsy A. Hirsch, Jessica A. Pollard, Bassem I. Razzouk, Kelly D. Getz, Richard Aplenc, E. Anders Kolb, Bonnie Ky, and Todd M. Cooper
- Subjects
CPX-351 ,pediatric acute myeloid leukemia (AML) ,relapse ,cardiotoxicity ,liposomal anthracycline ,cardiac biomarkers ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
IntroductionAnthracyclines are effective in treating acute myeloid leukemia (AML) but limited by cardiotoxicity. CPX-351, a liposomal daunorubicin and cytarabine, may provide therapeutic benefit with less cardiotoxicity. Acute changes in left ventricular systolic function and cardiac biomarkers were evaluated after a cycle of CPX-351 in children with relapsed AML treated on the phase 1/2 Children's Oncology Group study, AAML1421.MethodsSubjects received 135 units/m2/dose of CPX-351 on days 1, 3, and 5 as cycle 1. Echocardiograms were performed and centrally quantitated at baseline and at the end of cycle 1 (day 29 +/− 1 week). High sensitivity troponin (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were measured at baseline and serially through the end of cycle 1 (days 5, 8, 15, 22 and 29). Differences between baseline and post-CPX-351 echo/biomarker measures were analyzed using Wilcoxon signed rank tests. Linear regression was used to model post-CPX-351 left ventricular ejection fraction (LVEF) with cTnT/NT-proBNP at each time point, controlling for baseline LVEF. Cancer therapy related cardiac dysfunction (CTRCD) was defined as a decline in LVEF of ≥10%–
- Published
- 2024
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