Abstract

Acute myeloid leukemia (AML) is the result of dysregulating mutations within a multipotent myeloid stem/progenitor cell that result in uncontrolled cellular proliferation and differentiation arrest, compromising normal hematopoiesis, and typically manifesting with severe symptomatic pancytopenia. AML is a genetically complex disease with malignant clones most often born of varied chronological acquisition of mutations. Risk stratification and treatment decisions are increasingly informed by our understanding of this genetic framework. Cytogenetic and molecular genetic data are integrated with clinical, laboratory, and histopathologic data to provide more refined diagnostic and prognostic information specific for the individual. As our ability to describe this disease clinically, pathologically, and especially genetically becomes increasingly sophisticated, we expect progress in the development of targeted treatments and improved clinical outcomes.

Original languageEnglish
Title of host publicationAtlas of Diagnostic Hematology
PublisherElsevier
Pages110-141
Number of pages32
ISBN (Electronic)9780323567381
ISBN (Print)9780323567343
DOIs
StatePublished - 1 Jan 2020

Keywords

  • acute myeloid leukemia (AML)
  • acute promyelocytic leukemia (APL)
  • core-binding factor AML
  • fluorescence in situ hybridization (FISH)
  • karyotype
  • molecular genetic secondary AML
  • therapy-related AML

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