C/EBPα

Critical at the origin of leukemic transformation

Jae-Seok Roe, Christopher R. Vakoc

Research output: Contribution to journalShort survey

17 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1-4
Number of pages4
JournalJournal of Experimental Medicine
Volume211
Issue number1
DOIs
Publication statusPublished - 2014 Jan 1

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Acute Myeloid Leukemia
Oncogene Proteins
Transcription Factors
Myeloid Progenitor Cells
Hematologic Neoplasms
Oncogenes
Chromatin
Maintenance

All Science Journal Classification (ASJC) codes

  • Immunology
  • Immunology and Allergy

Cite this

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C/EBPα : Critical at the origin of leukemic transformation. / Roe, Jae-Seok; Vakoc, Christopher R.

In: Journal of Experimental Medicine, Vol. 211, No. 1, 01.01.2014, p. 1-4.

Research output: Contribution to journalShort survey

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N2 - 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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