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Article

Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer.

Genes & development - 15 Nov 2006

Bardeesy Nabeel, Cheng Kuang-Hung, Berger Justin H, Chu Gerald C, Pahler Jessica, Olson Peter, Hezel Aram F, Horner James, Lauwers Gregory Y, Hanahan Douglas, DePinho Ronald A

Abstract excerpt

SMAD4 is inactivated in the majority of pancreatic ductal adenocarcinomas (PDAC) with concurrent mutational inactivation of the INK4A/ARF tumor suppressor locus and activation of the KRAS oncogene. Here, using genetically engineered mice, we determined the impact of SMAD4 deficiency on the development of the pancreas and on the initiation and/or progression of PDAC-alone or in combination with PDAC--relevant...

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Topics

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Share to Carcinoma, Pancreatic Ductal
Share to Cyclin-Dependent Kinase Inhibitor p16

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genes, ras

Share to Pancreas

Share to Pancreatic Neoplasms

Share to Smad4 Protein

Share to Transforming Growth Factor beta

Share to Tumor Suppressor Protein p14ARF

Source

Open in PubMed Open full text

Identifiers

PMID: 17114584
DOI: 10.1101/gad.1478706
PMCID: PMC1635148

Genes

SMAD4
KRAS

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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