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Article

The acinar regulator Gata6 suppresses KrasG12V-driven pancreatic tumorigenesis in mice.

Gut - 1 Mar 2016

Martinelli Paola, Madriles Francesc, Cañamero Marta, Pau Enrique Carrillo-de Santa, Pozo Natalia Del, Guerra Carmen, Real Francisco X

Abstract excerpt

BACKGROUND AND AIMS: Gata6 is required to complete and maintain acinar differentiation in the mouse pancreas. Pancreas-specific Gata6 ablation during development causes extensive and persistent acinar-ductal metaplasia, which is considered an initial step of mutant KRas-driven carcinogenesis. Therefore, the Gata6-null pancreas might represent a tumour-prone environment. We investigated whether Gata6 plays a role...

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Share to Acinar Cells
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Carcinoma, Pancreatic Ductal

Share to GATA6 Transcription Factor

Share to Gene Expression Regulation, Neoplastic

Share to Mice, Transgenic

Share to Pancreatic Neoplasms

Share to Proto-Oncogene Proteins p21(ras)

Source

Identifiers

PMID: 25596178
DOI: 10.1136/gutjnl-2014-308042

Genes

EGFR
GATA6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

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