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Review
. 2017:962:151-173.
doi: 10.1007/978-981-10-3233-2_11.

RUNX1-ETO Leukemia

Shan Lin  1 , James C Mulloy  1 , Susumu Goyama  2
Affiliations
Review

RUNX1-ETO Leukemia

Shan Lin et al. Adv Exp Med Biol. 2017.

Abstract

AML1-ETO leukemia is the most common cytogenetic subtype of acute myeloid leukemia, defined by the presence of t(8;21). Remarkable progress has been achieved in understanding the molecular pathogenesis of AML1-ETO leukemia. Proteomic surveies have shown that AML-ETO forms a stable complex with several transcription factors, including E proteins. Genome-wide transcriptome and ChIP-seq analyses have revealed the genes directly regulated by AML1-ETO, such as CEBPA. Several lines of evidence suggest that AML1-ETO suppresses endogenous DNA repair in cells to promote mutagenesis, which facilitates acquisition of cooperating secondary events. Furthermore, it has become increasingly apparent that a delicate balance of AML1-ETO and native AML1 is important to sustain the malignant cell phenotype. Translation of these findings into the clinical setting is just beginning.

Keywords: AML1(RUNX1); AML1-ETO (RUNX1-ETO); Acute myeloid leukemia; DNA repair; Epigenetics; Signal transduction; Transcription factor complex.

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