ArticleOncogene2016
APC haploinsufficiency coupled with p53 loss sufficiently induces mucinous cystic neoplasms and invasive pancreatic carcinoma in mice.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Cell-Free DNA Hypermethylation in Patients with Acute Pancreatitis.International journal of molecular sciences · 2025Article
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- Integrated Workflow for the Label-Free Isolation and Genomic Analysis of Single Circulating Tumor Cells in Pancreatic Cancer.International journal of molecular sciences · 2022Article
- Cross-Talk between p53 and Wnt Signaling in Cancer.Biomolecules · 2022Review
- Stem cells and origins of cancer in the upper gastrointestinal tract.Cell stem cell · 2021Review
- Inhibition of β-Catenin Activity Abolishes LKB1 Loss-Driven Pancreatic Cystadenoma in Mice.International journal of molecular sciences · 2021Article
- Review
- Inactivation of APC Induces CD34 Upregulation to Promote Epithelial-Mesenchymal Transition and Cancer Stem Cell Traits in Pancreatic Cancer.International journal of molecular sciences · 2020Article
- Effect of Adenomatous Polyposis Coli Loss on Tumorigenic Potential in Pancreatic Ductal Adenocarcinoma.Cells · 2019Article
- Review
- Loss of the transcriptional repressor TGIF1 results in enhanced Kras-driven development of pancreatic cancer.Molecular cancer · 2019Article
- Conserved serum protein biomarkers associated with growing early colorectal adenomas.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- β-catenin-activated autocrine PDGF/Src signaling is a therapeutic target in pancreatic cancer.Theranostics · 2019Article
- Article
- Article
- Molecular Drivers of Pancreatic Cancer Pathogenesis: Looking Inward to Move Forward.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenomatous polyposis coli (APC), a tumor-suppressor gene critically involved in familial adenomatous polyposis, is integral in Wnt/β-catenin signaling and is implicated in the development of sporadic tumors of the distal gastrointestinal tract including pancreatic cancer (PC). Here we report for the first time that functional APC is required for the growth and maintenance of pancreatic islets and maturation. Subsequently, a non-Kras mutation-induced premalignancy mouse model was developed; in this model, APC haploinsufficiency coupled with p53 deletion resulted in the development of a distinct type of pancreatic premalignant precursors, mucinous cystic neoplasms (MCNs), exhibiting pathomechanisms identical to those observed in human MCNs, including accumulation of cystic fluid secreted by neoplastic and ovarian-like stromal cells, with 100% penetrance and the presence of hepatic and gastric metastases in >30% of the mice. The major clinical implications of this study suggest targeting the Wnt signaling pathway as a novel strategy for managing MCN.
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