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 language | English |
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Title of host publication | Atlas of Diagnostic Hematology |
Publisher | Elsevier |
Pages | 110-141 |
Number of pages | 32 |
ISBN (Electronic) | 9780323567381 |
ISBN (Print) | 9780323567343 |
DOIs | |
State | Published - 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