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Loss of Setd2 promote Kras-induced acinar-to-ductal metaplasia and epitheliamesenchymal transition during pancreatic carcinogenesis

GSE126302 Mus musculus Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing 10 samples Submitted 2020/08/02 Platform GPL21273
Summary
TCGA(PAAD) public database and PDAC tissue array with SETD2/H3K36me3 staining was used to investigate the clinical relevance of SETD2 in PDAC. Furthermore, to define the role of SETD2 in the carcinogenesis of PDAC, we crossed conditional Setd2 knockout mice (PdxcreSetd2flox/flox) together with with KrasG12D mice. Moreover, to examine the role of SETD2 after ductal metaplasia, Crisp/cas9 was used to deplete Setd2 in PDAC cells. RNA-seq and H3K36me3 Chip-seq were performed to uncover the mechanism.
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Direct links to NCBI, no account and no request form: the whole study as GSE126302_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 10 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA521511 and SRA study SRP184682. Searching any of these in the dataset finder brings you back here.

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