C/EBPα: Critical at the origin of leukemic transformation

Jae Seok Roe, Christopher R. Vakoc

Research output: Contribution to journalShort surveypeer-review

27 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1-4
Number of pages4
JournalJournal of Experimental Medicine
Issue number1
Publication statusPublished - 2014 Jan

All Science Journal Classification (ASJC) codes

  • Medicine(all)


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