C/EBPα: critical at the origin of leukemic transformation

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


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.

Publication types

  • Review

MeSH terms

  • CCAAT-Enhancer-Binding Protein-alpha / metabolism*
  • Cell Transformation, Neoplastic / metabolism*
  • Feedback, Physiological / physiology
  • Humans
  • Leukemia, Myeloid, Acute / physiopathology*
  • Models, Biological
  • Myeloid-Lymphoid Leukemia Protein / metabolism
  • Myelopoiesis / physiology*


  • CCAAT-Enhancer-Binding Protein-alpha
  • Myeloid-Lymphoid Leukemia Protein