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J Exp Med. 2014 Jan 13;211(1):1-4. doi: 10.1084/jem.20132530. Epub 2014 Jan 6.

C/EBPα: critical at the origin of leukemic transformation.

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  • 1the Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724.

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.

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