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Loss of Setd2 promotes Kras-induced acinar-to-ductal metaplasia and epithelia–mesenchymal transition...

Loss of Setd2 promotes Kras-induced acinar-to-ductal metaplasia and epithelia–mesenchymal transition...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_journals_2372614724

Loss of Setd2 promotes Kras-induced acinar-to-ductal metaplasia and epithelia–mesenchymal transition during pancreatic carcinogenesis

About this item

Full title

Loss of Setd2 promotes Kras-induced acinar-to-ductal metaplasia and epithelia–mesenchymal transition during pancreatic carcinogenesis

Publisher

England: BMJ Publishing Group Ltd and British Society of Gastroenterology

Journal title

Gut, 2020-04, Vol.69 (4), p.715-726

Language

English

Formats

Publication information

Publisher

England: BMJ Publishing Group Ltd and British Society of Gastroenterology

More information

Scope and Contents

Contents

ObjectiveSETD2, the sole histone H3K36 trimethyltransferase, is frequently mutated or deleted in human cancer, including pancreatic ductal adenocarcinoma (PDAC). However, whether SETD2/H3K36me3 alteration results in PDAC remains largely unknown.DesignTCGA(PAAD) public database and PDAC tissue array with SETD2/H3K36me3 staining were used to investig...

Alternative Titles

Full title

Loss of Setd2 promotes Kras-induced acinar-to-ductal metaplasia and epithelia–mesenchymal transition during pancreatic carcinogenesis

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_proquest_journals_2372614724

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_journals_2372614724

Other Identifiers

ISSN

0017-5749

E-ISSN

1468-3288

DOI

10.1136/gutjnl-2019-318362

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