ArticleScientific reports2016
TGF-β1 promotes acinar to ductal metaplasia of human pancreatic acinar cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- PGC1α-Mediated Metabolic Reprogramming Drives the Stemness of Pancreatic Precursor Lesions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Pooled it
- Acinar-ductal metaplasia in pancreatitis and pancreatic ductal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- NF2 loss malignantly transforms human pancreatic acinar cells and enhances cell fitness under environmental stress.The Journal of clinical investigation · 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
- The complex interplay between diabetes mellitus and pancreatic carcinogenesis: deciphering multifactorial mechanisms and identifying emerging therapeutic vulnerabilities.Cell & bioscience · 2025Review
- The scRNA-sequencing landscape of pancreatic ductal adenocarcinoma revealed distinct cell populations associated with tumor initiation and progression.Genes & diseases · 2025Article
- Article
- Subtype Transdifferentiation in Human Cancer: The Power of Tissue Plasticity in Tumor Progression.Cells · 2024Review
- Reconstitution of human PDAC using primary cells reveals oncogenic transcriptomic features at tumor onset.Nature communications · 2024Article
- TGFβ and Hippo Signaling Pathways Coordinate to Promote Acinar to Ductal Metaplasia in Human Pancreas.Cells · 2024Article
- Krüppel-like Factor 5 Plays an Important Role in the Pathogenesis of Chronic Pancreatitis.Cancers · 2023Article
- ST6GAL1 sialyltransferase promotes acinar to ductal metaplasia and pancreatic cancer progression.JCI insight · 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
- Muc4 loss mitigates epidermal growth factor receptor activity essential for PDAC tumorigenesis.Oncogene · 2023Article
- Transcriptional Profile of Human Pancreatic Acinar Ductal Metaplasia.Gastro hep advances · 2023Article
- Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia.Cell death discovery · 2022Article
- Salivary gland organoid culture maintains distinct glandular properties of murine and human major salivary glands.Nature communications · 2022Article
- Encapsulation of Primary Salivary Gland Acinar Cell Clusters and Intercalated Ducts (AIDUCs) within Matrix Metalloproteinase (MMP)-Degradable Hydrogels to Maintain Tissue Structure and Function.Advanced healthcare materials · 2022Article
- Molecular signaling in pancreatic ductal metaplasia: emerging biomarkers for detection and intervention of early pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Animal studies suggest that pancreatitis-induced acinar-to-ductal metaplasia (ADM) is a key event for pancreatic ductal adenocarcinoma (PDAC) initiation. However, there has not been an adequate system to explore the mechanisms of human ADM induction. We have developed a flow cytometry-based, high resolution lineage tracing method and 3D culture system to analyse ADM in human cells. In this system, well-known mouse ADM inducers did not promote ADM in human cells. In contrast, TGF-β1 efficiently converted human acinar cells to duct-like cells (AD) in a SMAD-dependent manner, highlighting fundamental differences between the species. Functionally, AD cells gained transient proliferative capacity. Furthermore, oncogenic KRAS did not induce acinar cell proliferation, but did sustain the proliferation of AD cells, suggesting that oncogenic KRAS requires ADM-associated-changes to promote PDAC initiation. This ADM model provides a novel platform to explore the mechanisms involved in the development of human pancreatic diseases.
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Registered trials
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.