ArticleeLife2015
The acinar differentiation determinant PTF1A inhibits initiation of pancreatic ductal adenocarcinoma.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 176 citations in OpenAlex.
- Acinar-Derived Organoids Reveal Stage-Specific Control of Acinar Plasticity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
- Acinar-specific loss of activating transcription factor 3 restricts KRASCell death discovery · 2025Article
- Embryonic Origins of Cancer: Insights from Double Homeobox 4 Regulation.Biomolecules · 2025Review
- DNA methylation memory of pancreatic acinar-ductal metaplasia transition state altering Kras-downstream PI3K and Rho GTPase signaling in the absence of Kras mutation.Genome medicine · 2025Article
- Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis.Nature genetics · 2025Article
- Stage-Specific Tumoral Gene Expression Profiles of Black and White Patients with Colon Cancer.Annals of surgical oncology · 2025Article
- Cancer research and the mainstream of biology.Frontiers in cell and developmental biology · 2025Review
- ROR2 Regulates Cellular Plasticity in Pancreatic Neoplasia and Adenocarcinoma.Cancer discovery · 2024Article
- Diagnostic and Prognostic Markers for Pancreatitis and Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2024Article
- Article
- Rare, Tightly-Bound, Multi-Cellular Clusters in the Pancreatic Ducts of Adult Mice Function Like Progenitor Cells and Survive and Proliferate After Acinar Cell Injury.Stem cells (Dayton, Ohio) · 2024Article
- Activation of ductal progenitor-like cells from adult human pancreas requires extracellular matrix protein signaling.iScience · 2024Article
- Subtype Transdifferentiation in Human Cancer: The Power of Tissue Plasticity in Tumor Progression.Cells · 2024Review
- Cancer as a Disease of Development Gone Awry.Annual review of pathology · 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
- Pancreatic Ubap2 deletion regulates glucose tolerance, inflammation, and protection from cerulein-induced pancreatitis.Cancer letters · 2023Article
- Pancreatic acinar cell fate relies on system xCell death & disease · 2023Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Understanding the initiation and progression of pancreatic ductal adenocarcinoma (PDAC) may provide therapeutic strategies for this deadly disease. Recently, we and others made the surprising finding that PDAC and its preinvasive precursors, pancreatic intraepithelial neoplasia (PanIN), arise via reprogramming of mature acinar cells. We therefore hypothesized that the master regulator of acinar differentiation, PTF1A, could play a central role in suppressing PDAC initiation. In this study, we demonstrate that PTF1A expression is lost in both mouse and human PanINs, and that this downregulation is functionally imperative in mice for acinar reprogramming by oncogenic KRAS. Loss of Ptf1a alone is sufficient to induce acinar-to-ductal metaplasia, potentiate inflammation, and induce a KRAS-permissive, PDAC-like gene expression profile. As a result, Ptf1a-deficient acinar cells are dramatically sensitized to KRAS transformation, and reduced Ptf1a greatly accelerates development of invasive PDAC. Together, these data indicate that cell differentiation regulators constitute a new tumor suppressive mechanism in the pancreas.
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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.