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Publication

Arid1a restrains Kras-dependent changes in acinar cell identity.

eLife | 2018

Mutations in members of the SWI/SNF chromatin remodeling family are common events in cancer, but the mechanisms whereby disruption of SWI/SNF components alters tumorigenesis remain poorly understood. To model the effect of loss of function mutations in the SWI/SNF subunit Arid1a in pancreatic ductal adenocarcinoma (PDAC) initiation, we directed shRNA triggered, inducible and reversible suppression of Arid1a to the mouse pancreas in the setting of oncogenic KrasG12D. Arid1a cooperates with Kras in the adult pancreas as postnatal silencing of Arid1a following sustained KrasG12D expression induces rapid and irreversible reprogramming of acinar cells into mucinous PDAC precursor lesions. In contrast, Arid1a silencing during embryogenesis, concurrent with KrasG12D activation, leads to retention of acinar cell fate. Together, our results demonstrate Arid1a as a critical modulator of Kras-dependent changes in acinar cell identity, and underscore an unanticipated influence of timing and genetic context on the effects of SWI/SNF complex alterations in epithelial tumorigenesis.

Pubmed ID: 30014851 RIS Download

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Associated grants

Agency: NIH HHS, United States
Id: U54 OD020355
Agency: NCI NIH HHS, United States
Id: CA13106
Agency: Howard Hughes Medical Institute, United States
Agency: NCI NIH HHS, United States
Id: F32 CA177072
Agency: NCI NIH HHS, United States
Id: P30 CA008748
Agency: NCI NIH HHS, United States
Id: 1F32CA177072-01
Agency: NCI NIH HHS, United States
Id: P01 CA013106
Agency: NCI NIH HHS, United States
Id: Cancer Center Core Grants P30-CA008748
Agency: NCI NIH HHS, United States
Id: R01 CA195787

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