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• W2606071743 startingPage "151" @default.
• W2606071743 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." @default.
• W2606071743 created "2017-04-28" @default.
• W2606071743 creator A5000842818 @default.
• W2606071743 creator A5086241483 @default.
• W2606071743 creator A5087496453 @default.
• W2606071743 date "2017-01-01" @default.
• W2606071743 modified "2023-10-16" @default.
• W2606071743 title "RUNX1-ETO Leukemia" @default.
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