Effects of the leukemia-associated AML1-ETO protein on hematopoietic stem and progenitor cells

Stephen D. Nimer, Malcolm A.S. Moore

Research output: Contribution to journalReview articlepeer-review

46 Scopus citations

Abstract

Insights into the pathogenesis of human leukemia have relied heavily on studies of the identified chromosomal translocations found in this group of malignant diseases. Acquired, balanced translocations in acute myclogenous leukemia (AML) generally involve transcriptional regulatory genes, whereas in the myeloproliferative disorders tyrosine kinases are frequently involved. These rearrangements alter the function of at least one and often both of the involved genes. In this review, we focus on the AML1-ETO (a.k.a. RUNX1-ETO) fusion protein, which is found in t(8;21) + AML. Expression of AML1-ETO in human hematopoietic stem cells (HSCs) preferentially enhances their maintenance, as opposed to their differentiation. The direct effects of AML1-ETO on human and murine HSCs, and the potentially cooperating events that may contribute to its leukemogenic properties, are discussed.

Original languageEnglish (US)
Pages (from-to)4249-4254
Number of pages6
JournalOncogene
Volume23
Issue number24
DOIs
StatePublished - May 24 2004
Externally publishedYes

Keywords

  • AML
  • AML1-ETO
  • Stem cell biology
  • Transcription factors

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

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