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- W4386811890 abstract "Abstract Acute myeloid leukemia (AML) with the t(7;12)(q36;p13) translocation occurs only in very young children and has a poor outcome. The expected oncofusion between breakpoint partners ( MNX1 and ETV6 ) has only been reported in a subset of cases. However, a universal feature is the strong transcript and protein expression of MNX1 , a homeobox transcription factor that is normally not expressed in hematopoietic cells. Here, we map the translocation breakpoints on chromosomes 7 and 12 in affected patients to a region downstream of MNX1 and either introns 1 or 2 of ETV6 . The frequency of MNX1 overexpression in pediatric AML (n=1556, own and published data) is 2.4% and occurs predominantly in t(7;12)(q36;p13) AML. Chromatin interaction assays in a t(7;12)(q36;p13) iPSC cell line model unravel an enhancer-hijacking event that explains MNX1 overexpression in hematopoietic cells. Our data suggest that enhancer-hijacking is a more common and overlooked mechanism for structural rearrangement-mediated gene activation in AML." @default.
- W4386811890 created "2023-09-18" @default.
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- W4386811890 date "2023-09-17" @default.
- W4386811890 modified "2023-10-03" @default.
- W4386811890 title "Altered enhancer-promoter interaction leads to<i>MNX1</i>expression in pediatric acute myeloid leukemia with t(7;12)(q36;p13)" @default.
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- W4386811890 doi "https://doi.org/10.1101/2023.09.13.557546" @default.
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