title: C/EBPα: critical at the origin of leukemic transformation.
abstract: Acute myeloid leukemia (AML) is a hematopoietic malignancy characterized by clonal expansion of myeloid progenitor cells. A major mechanistic theme in AML biology is the extensive collaboration among fusion oncoproteins, transcription factors, and chromatin regulators to initiate and sustain a transformed cellular state. A new study in this issue describes how the C/EBPα transcription factor is crucial for the initiation of AML induced by MLL fusion oncoproteins, but is entirely dispensable for the maintenance of established disease. These observations provide a unique glimpse into the pioneer round of regulatory events that are critical at the origin of AML formation. Furthermore, this study implies the existence of oncogene-induced positive feedback loops capable of bypassing the continuous need for certain regulators to propagate disease.
authors.affiliation: the Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724.
authors.forename: Jae-Seok
authors.initials: JS
authors.lastname: Roe
authors.forename: Christopher R
authors.initials: CR
authors.lastname: Vakoc
mesh_terms: D022763:CCAAT-Enhancer-Binding Protein-alpha / Q000378:metabolism*; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D025461:Feedback, Physiological / Q000502:physiology; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000503:physiopathology*; D008954:Models, Biological; D051788:Myeloid-Lymphoid Leukemia Protein / Q000378:metabolism; D038042:Myelopoiesis / Q000502:physiology*
chemical_list: D022763:CCAAT-Enhancer-Binding Protein-alpha; D051788:Myeloid-Lymphoid Leukemia Protein