ArticleGastroenterology2007
In vivo lineage tracing defines the role of acinar-to-ductal transdifferentiation in inflammatory ductal metaplasia.
Article in Gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.
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Who cites it
166 citing papers in PubMed, 269 citations in OpenAlex.
- Acinar-Derived Organoids Reveal Stage-Specific Control of Acinar Plasticity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026Review
- Presence of Tuft Cells Expressing Hematopoietic Prostaglandin D Synthase in Acinar-to-Ductal Metaplasia in Human Obstructive Pancreatitis.Current issues in molecular biology · 2026Article
- Cystic lesions and their role in pancreatic cancer risk stratification.Translational oncology · 2026Review
- Spatiotemporal control of SMARCA5 by a MAPK-RUNX1 axis distinguishes mutant KRAS-driven pancreatic malignancy from tissue regeneration.Nature cancer · 2026Article
- Transcriptomic Analyses of Normal Human Pancreata Reveal the Presence of Cancer Subtypes that Correlate with Acinar Ductal Metaplasia and Donor Ancestry.Cancer research communications · 2026Article
- Stem/progenitor cell dynamics during salivary gland development and regeneration demonstrated by the double pulse-chase paradigm.Regenerative therapy · 2025Article
- Immunohistochemical Demonstration of Tuft Cells in Human Acinar-to-Ductal Metaplasia and Pancreatic Intraepithelial Neoplasia.Biomedicines · 2025Article
- Joint representation and visualization of derailed cell states with Decipher.Genome biology · 2025Article
- Therapeutic targeting of FOSL1 and RELA-dependent transcriptional mechanisms to suppress pancreatic cancer metastasis.Cell death & disease · 2025Article
- Anti-proteolytic regulation of KRAS by USP9X/NDRG3 in KRAS-driven cancer development.Nature communications · 2025Article
- The role of inflammatory factors in the tumor microenvironment of pancreatic cancer.Frontiers in immunology · 2025Review
- PRRX1 Has Functional Roles in Pancreatic Acinar to Ductal Metaplasia and Carcinogenesis.Cellular and molecular gastroenterology and hepatology · 2025Article
- Small molecular weight epigenetic inhibitors modulate the extracellular matrix during pancreatic acinar ductal metaplasia.Biochemical and biophysical research communications · 2024Article
- FRA1 controls acinar cell plasticity during murine KrasDevelopmental cell · 2024Article
- ROR2 Regulates Cellular Plasticity in Pancreatic Neoplasia and Adenocarcinoma.Cancer discovery · 2024Article
- Tumor initiation and early tumorigenesis: molecular mechanisms and interventional targets.Signal transduction and targeted therapy · 2024Review
- Diagnostic Challenges during Inflammation and Cancer: Current Biomarkers and Future Perspectives in Navigating through the Minefield of Reactive versus Dysplastic and Cancerous Lesions in the Digestive System.International journal of molecular sciences · 2024Review
- ROR2 regulates cellular plasticity in pancreatic neoplasia and adenocarcinoma.bioRxiv : the preprint server for biology · 2024Article
- Epigenetic small-molecule screen for inhibition and reversal of acinar ductal metaplasia in mouse pancreatic organoids.Frontiers in pharmacology · 2024Article
106 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
BACKGROUND &
aimsChronic injury results in regeneration of normal pancreatic tissue and formation of a metaplasia of ductal phenotype. Metaplastic ductal lesions are seen in pancreatitis as well as in specimens of pancreatic cancer and are thought to represent a condition with increased risk of neoplasia. Acinar-to-ductal transdifferentiation is thought to be the source of this metaplasia. This has been suggested for flat duct-like lesions called tubular complexes and for lesions exhibiting a mucinous metaplasia. However, available studies are based on interpretation of static data rather than on direct evidence. Transdifferentiation from acinar to ductal cells has never been confirmed in the adult pancreas.
methodsHere, we use Cre-loxP-based genetic lineage tracing in vivo to investigate whether transdifferentiation of acinar cells contributes to regeneration and metaplasia in pancreatitis.
resultsThe results show that transdifferentiation does not play a role in regeneration of normal tissue. Acinar cells are regenerated by preexisting acinar cells and not from other cell types. Three different types of metaplastic ductal lesions are observed and analyzed. Whereas the majority of metaplastic lesions are not of acinar origin, acinar-to-ductal transdifferentiation is identified in a minority of mucinous metaplastic lesions.
conclusionsHere, we provide direct evidence that acinar-to-ductal transdifferentiation occurs in the adult pancreas in vivo. However, it accounts for only a minority of metaplastic lesions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.