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Genetic and Genomics in Clinical Hematology, III: Acute Leukemias 

Genetic and Genomics in Clinical Hematology, III: Acute Leukemias
Chapter:
Genetic and Genomics in Clinical Hematology, III: Acute Leukemias
Author(s):

Kenneth Mills

DOI:
10.1093/med/9780199896028.003.0027
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date: 31 May 2020

Acute myeloid leukaemia (AML) is a genetically heterogeneous disorder characterized by arrest of differentiation in the myeloid lineage coupled with an accumulation of immature progenitors in the bone marrow, resulting in hematopoietic failure. AML is the most common form of acute leukemia in adults; AML accounts for only around 10% of paediatric leukemia cases. The cause of AML is unknown in most cases, but the development has been strongly linked to radiation, chemical exposure (benzene), or prior use of alkylating agents, working in the background of several genes predisposing to triggering leukemogenesis. Some AML patients have evolved from a prior hematological disorder, e.g., chronic myeloid leukemia (CML), Myelodysplastic syndrome (MDS) or myeloproliferative neoplasm. Patients with MDS may develop AML; approximately 25% of AML patients have a previous history of MDS, this leukemia are generally designated as secondary leukemia and are of interest due to the probable multiple genetic aberrations required for the evolution into AML. In recent years, an increasing number of gene mutations, deregulated expression of genes and noncoding RNAs (miRNAs) and epigenetic changes have been identified which has added to the molecular heterogeneity of the disease

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