Journal
ONCOGENE
Volume 23, Issue 24, Pages 4249-4254Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1207673
Keywords
AML; AML1-ETO; stem cell biology; transcription factors
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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.
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