Journal
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
Volume 11, Issue 4, Pages -Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a034975
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Funding
- National Cancer Institute [PS-OC U54 CA143869-05, R35 CA197594-01A1, R01 CA216421]
- Leukemia & Lymphoma Society Translational Research Foundation [6499-17]
- Memorial Sloan Kettering Cancer Center Core Grant [P30 CA008748]
- VeloSano Catalyst Award
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AML is characterized by genetic and epigenetic aberrations, with mutations acquired stepwise. Understanding the pathogenesis of AML informs the development of prognostic models and therapeutic strategies.
Acute myeloid leukemia (AML) is characterized by attenuation of lineage differentiation trajectories that results in impaired hematopoiesis and enhanced self-renewal. To date, sequencing studies have provided a rich landscape of information on the somatic mutations that contribute to AML pathogenesis. These studies show that most AML genomes harbor relatively fewer mutations, which are acquired in a stepwise manner. Our understanding of the genetic basis of leukemogenesis informs a broader understanding of what initiates and maintains the AML clone and informs the development of prognostic models and mechanism-based therapeutic strategies. Here, we explore the current knowledge of genetic and epigenetic aberrations in AML pathogenesis and how recent studies are expanding our knowledge of leukemogenesis and using this to accelerate therapeutic development for AML patients.
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