Courtney DiNardo1, Curtis Lachowiez2. 1. Department of Leukemia, UT MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX, 77030, USA. cdinardo@mdanderson.org. 2. Division of Cancer Medicine, MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX, 77030, USA.
Abstract
PURPOSE OF REVIEW: Awareness of the molecular landscape of AML has improved AML care over the last 5 years. This review summarizes updates regarding the diagnostic and therapeutic relevance of key mutations in AML. RECENT FINDINGS: Molecular mutations in genes including NPM1, CEBPA, FLT3, IDH1/2, TP53, RUNX1, and ASXL1 provide important prognostic and/or therapeutic information in AML, including best treatment strategies, transplant recommendations, and significance of MRD detection. Mutational analysis has led to the recognition of new entities including hereditary leukemia syndromes and clonal hematopoiesis of indeterminate potential (CHIP). FLT3 and IDH1/2 mutations are the focus of targeted therapies in the treatment of AML. Advances in the molecular characterization of AML have provided an improved understanding of leukemogenesis and AML risk stratification, improved disease monitoring techniques, optimized therapeutic strategies, and have led to the development of novel molecular-targeted therapeutics. Ongoing genomic advances will continue to improve upon the outcome of patients with AML.
PURPOSE OF REVIEW: Awareness of the molecular landscape of AML has improved AML care over the last 5 years. This review summarizes updates regarding the diagnostic and therapeutic relevance of key mutations in AML. RECENT FINDINGS: Molecular mutations in genes including NPM1, CEBPA, FLT3, IDH1/2, TP53, RUNX1, and ASXL1 provide important prognostic and/or therapeutic information in AML, including best treatment strategies, transplant recommendations, and significance of MRD detection. Mutational analysis has led to the recognition of new entities including hereditary leukemia syndromes and clonal hematopoiesis of indeterminate potential (CHIP). FLT3 and IDH1/2 mutations are the focus of targeted therapies in the treatment of AML. Advances in the molecular characterization of AML have provided an improved understanding of leukemogenesis and AML risk stratification, improved disease monitoring techniques, optimized therapeutic strategies, and have led to the development of novel molecular-targeted therapeutics. Ongoing genomic advances will continue to improve upon the outcome of patients with AML.
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