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The Molecular Pathogenesis of Acute Myeloid Leukemia

Kiran Tawana1, Csaba Bödör2, Jamie Cavenagh3, Michael Jenner1, and Jude Fitzgibbon1

Acute myeloid leukemia (AML) is the most common form of aggressive leukemia in adults. In the UK, there are approximately 2000 new cases per year, with the majority occurring in older patients (>60 years of age). It is a complex disease that may occur as a de novo neoplasm, secondary to the transformation of an antecedent myeloid malignancy such as a chronic myeloproliferative neoplasm or myelodysplasia (MDS), or as a complication of exposure to DNA-damaging agents, such as chemotherapy, for unrelated malignancies. The disease is characterized by the accumulation of immature blast cells within the bone marrow, with overspill of a variable quantity into the peripheral blood. These blasts arise from leukemia-initiating cells (LICs), which are hematopoietic stem cells (HSCs) or myeloid progenitors that maintain self-renewal capacity and have undergone malignant transformation because of their accumulation of genetic aberrations [1,2].

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