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Biology of Acute Myeloid Leukemia

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Childhood Leukemia

Part of the book series: Pediatric Oncology ((PEDIATRICO))

Abstract

AML is a heterogeneous and complex disease that is the culmination of the interaction between genetic and epigenetic alterations in the hematopoietic progenitors, leading to dysregulation of multiple critical signal transduction pathways, resulting in hematopoietic insufficiency due to the accumulation of immature myeloid progenitors. Despite identification of numerous cytogenetic, molecular and epigenetic alterations in AML, attempts at defining a unifying disease causing event in AML have failed. In contrast to chronic myeloid leukemia (CML), in which evolution of a single event (BCR-ABL translocation) is causally associated with disease pathogenesis, such a single step process does not appear to be responsible in AML pathogenesis. In vivo studies have demonstrated that common cytogenetic alterations such as t(8;21) or inv(16) that are highly associated with AML are not sufficient for the disease pathogenesis. These findings led to the hypothesis that evolution of AML may require multiple genetic changes and that the disease may require cooperation between two or more alterations.

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Arceci, R.J., Meshinchi, S. (2011). Biology of Acute Myeloid Leukemia. In: Reaman, G., Smith, F. (eds) Childhood Leukemia. Pediatric Oncology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-13781-5_3

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