ArticleThe American journal of pathology2007
Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
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Who cites it
140 citing papers in PubMed.
- Acinar-Derived Organoids Reveal Stage-Specific Control of Acinar Plasticity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-Dose L-Lysine-Induced Pancreatitis Followed by Pancreatic Neoplastic Progression in AdultMethods and protocols · 2026Article
- Acinar-ductal metaplasia in pancreatitis and pancreatic ductal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- ALDH1L2 regulates reactive oxygen species and acinar-to-ductal metaplasia in the pancreas.Nature metabolism · 2026Article
- Cellular states associated with metastatic organotropism and survival in patients with pancreatic ductal adenocarcinoma.Nature genetics · 2025Article
- Anti-proteolytic regulation of KRAS by USP9X/NDRG3 in KRAS-driven cancer development.Nature communications · 2025Article
- Suppression of dystroglycan function accompanies pancreatic acinar-to-ductal metaplasia and favours dysplasia development.The Journal of pathology · 2024Article
- How much do we know about the metastatic process?Clinical & experimental metastasis · 2024Review
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- Article
- Identification and analysis of pancreatic intraepithelial neoplasia: opportunities and challenges.Frontiers in endocrinology · 2024Review
- Oncogenic KRAS, Mucin 4, and Activin A-Mediated Fibroblast Activation Cooperate for PanIN Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Acinar-to-Ductal Metaplasia (ADM): On the Road to Pancreatic Intraepithelial Neoplasia (PanIN) and Pancreatic Cancer.International journal of molecular sciences · 2023Review
- Comprehensive DNA Methylation Analysis Indicates That Pancreatic Intraepithelial Neoplasia Lesions Are Acinar-Derived and Epigenetically Primed for Carcinogenesis.Cancer research · 2023Article
- Key transcriptional effectors of the pancreatic acinar phenotype and oncogenic transformation.PloS one · 2023Article
- Recent advances of three-dimensional bioprinting technology in hepato-pancreato-biliary cancer models.Frontiers in oncology · 2023Review
- CODA: quantitative 3D reconstruction of large tissues at cellular resolution.Nature methods · 2022Article
- Molecular signaling in pancreatic ductal metaplasia: emerging biomarkers for detection and intervention of early pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Article
- Cell Type of Pancreatic Ductal Adenocarcinoma Origin: Implications for Prognosis and Clinical Outcomes.Visceral medicine · 2022Review
80 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
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Abstract
A number of studies have shown that pancreatic ductal adenocarcinoma develops through precursor lesions termed pancreatic intraepithelial neoplasia (PanIN). PanINs are thought to initiate in the small ducts of the pancreas through activating mutations in the KRAS proto-oncogene. What remains unanswered is the identification of the individual cell type(s) that contributes to pancreatic ductal adenocarcinoma formation. To follow the cellular and molecular changes that occur in acinar and duct cell properties on Kras(G12D) expression, we took advantage of LSL-Kras(G12D/+)/p48(Cre/+) mice, which faithfully mimic the human disease. In young animals (4 weeks), the predominant cellular alteration in the exocrine pancreas was acinar metaplasia in which individual acini consisted of acinar cells and duct-like cells. Metaplastic acinar structures were highly proliferative, expressed Notch target genes, and exhibited mosaic expression patterns for epidermal growth factor receptor, ErbB2, and pErk. This expression pattern paralleled the expression pattern detected in mouse PanINs, suggesting that mouse PanINs and acinar-ductal metaplasia follow similar molecular pathways. Indeed, immunofluorescence studies confirmed the presence of acinar cells within mPanIN lesions, raising the possibility that Kras(G12D)-induced mPanINs develop from acinar cells that undergo acinar-ductal metaplasia. Identification of an acinar contribution to PanIN formation offers new directions for successful targeted therapeutic approaches to combat this disease.
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