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Oncogenic pathways of AML1-ETO in acute myeloid leukemia: multifaceted manipulation of marrow maturation Elagib KE; Goldfarb ANCancer Lett 2007[Jun]; 251 (2): 179-86The leukemic fusion protein AML1-ETO occurs frequently in human acute myeloid leukemia (AML) and has received much attention over the past decade. An initial model for its pathogenetic effects emphasized the conversion of a hematopoietic transcriptional activator, RUNX1 (or AML1), into a leukemogenic repressor which blocked myeloid differentiation at the level of target gene regulation. This view has been absorbed into a larger picture of AML1-ETO pathogenesis, encompassing dysregulation of hematopoietic stem cell homeostasis at several mechanistic levels. Recent reports have highlighted a multifaceted capacity of AML1-ETO directly to inhibit key hematopoietic transcription factors that function as tumor suppressors at several nodal points during hematopoietic differentiation. A new model is presented in which AML1-ETO coordinates expansion of the stem cell compartment with diminished lineage commitment and with genome instability.|*Hematopoiesis[MESH]|Acute Disease[MESH]|Animals[MESH]|Bone Marrow/*physiology[MESH]|Cell Differentiation[MESH]|Core Binding Factor Alpha 2 Subunit/*metabolism[MESH]|Hematopoietic Stem Cells/physiology[MESH]|Humans[MESH]|Leukemia, Myeloid/*metabolism[MESH]|Models, Biological[MESH]|Mutation[MESH]|Oncogene Proteins, Fusion/*metabolism[MESH]|RUNX1 Translocation Partner 1 Protein[MESH]|Tumor Suppressor Proteins/drug effects[MESH] |
