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Paradigm Test Set aCGH Array

ABSTRACT: aCGH data was used in Paradigm analysis for exploration of networks affected by copy number and gene expression changes based on mutation spectra of recurrently mutated genes in breast cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35189 | GEO | 2012/06/21

SECONDARY ACCESSION(S): PRJNA155959

REPOSITORIES: GEO

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Paradigm Test Set aCGH Array

Project description:aCGH data was used in Paradigm analysis for exploration of networks affected by copy number and gene expression changes based on mutation spectra of recurrently mutated genes in breast cancer. 124 patients including 3 Pre-Operative Letrozole and 43 Z1031 patients were arrayed and analyzed

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Project description:The myeloid transcription factor CEBPA is recurrently biallelically mutated (i.e., double mutated; CEBPADM) in acute myeloid leukemia (AML); with a combination of hypermorphic N-terminal mutations (CEBPANT), promoting expression of the leukemia-associated p30 isoform, and amorphic C-terminal mutations. CEBPADM AML features recurrent co‑occurring mutations; however, insight into the underlying mechanisms for the co-mutational spectra is incomplete. By combining transcriptomic and epigenomic analyses of data from CEBPA-TET2-co-mutant patients with experimental models thereof, we identify GATA2 as a conserved target of the CEBPA-TET2 mutational axis, providing a rationale for the mutational spectra in CEBPADM AML. Mechanistically, we suggest that elevated CEBPA levels, driven by the CEBPANT, mediate recruitment of TET2 to the GATA2 distal hematopoietic enhancer and thereby increase GATA2 expression. Conversely, CEBPADM AML gains a competitive advantage by loss of TET2; decreasing GATA2 promoter demethylation and re-balancing GATA2 levels. Further, demethylating treatment of CEBPA-TET2-co-mutant AML restores GATA2 levels, and prolongs disease latency.

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