ArticleProceedings of the National Academy of Sciences of the United States of America2007
Beta cell transdifferentiation does not contribute to preneoplastic/metaplastic ductal lesions of the pancreas by genetic lineage tracing in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- Deciphering cellular plasticity in pancreatic cancer for effective treatments.Cancer metastasis reviews · 2024Review
- Article
- Molecular signaling in pancreatic ductal metaplasia: emerging biomarkers for detection and intervention of early pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- The cellular origins of cancer with particular reference to the gastrointestinal tract.International journal of experimental pathology · 2020Review
- Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2017Review
- β-cell replacement sources for type 1 diabetes: a focus on pancreatic ductal cells.Therapeutic advances in endocrinology and metabolism · 2016Review
- Hyperglycaemia attenuates in vivo reprogramming of pancreatic exocrine cells to beta cells in mice.Diabetologia · 2016Article
- Stem cells versus plasticity in liver and pancreas regeneration.Nature cell biology · 2016Review
- Pancreatic duct glands (PDGs) are a progenitor compartment responsible for pancreatic ductal epithelial repair.Stem cell research · 2015Article
- Spatiotemporal proteomic analyses during pancreas cancer progression identifies serine/threonine stress kinase 4 (STK4) as a novel candidate biomarker for early stage disease.Molecular & cellular proteomics : MCP · 2014Article
- Early epigenetic downregulation of WNK2 kinase during pancreatic ductal adenocarcinoma development.Oncogene · 2014Article
- ALDH1B1 is a potential stem/progenitor marker for multiple pancreas progenitor pools.Developmental biology · 2013Article
- Review
- The pathobiological impact of cigarette smoke on pancreatic cancer development (review).International journal of oncology · 2012Review
- Tamoxifen-Induced Cre-loxP Recombination Is Prolonged in Pancreatic Islets of Adult Mice.PloS one · 2012Article
- From tissue turnover to the cell of origin for pancreatic cancer.Nature reviews. Gastroenterology & hepatology · 2011Review
- Stat3 and MMP7 contribute to pancreatic ductal adenocarcinoma initiation and progression.Cancer cell · 2011Article
- Pancreatic duct glands are distinct ductal compartments that react to chronic injury and mediate Shh-induced metaplasia.Gastroenterology · 2010Article
- Article
- Heterogeneity in mitotic activity and telomere length implies an important role of young islets in the maintenance of islet mass in the adult pancreas.Endocrinology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory injury to the pancreas results in regeneration of normal tissue and formation of metaplastic lesions of a ductal phenotype. These metaplastic ductal lesions (MDL) are called tubular complexes (TC), mucinous metaplasia, or pancreatic intraepithelial neoplasia. Because they are regularly found in chronic pancreatitis and pancreatic cancer, their formation is thought to represent a step in inflammation-mediated carcinogenesis. Despite these lesions' ductal character, their origin is controversial. All known pancreatic cell lineages have been suggested as the origin. In vitro studies suggest that differentiated cells in the pancreas remain highly plastic and can transdifferentiate as a mechanism of regeneration and metaplasia. In vivo studies suggest that islets, specifically beta cells, may be the cell of origin. However, in vitro studies are subject to ductal cell contamination, and previous in vivo studies interpret static data rather than direct evidence. Using genetic lineage tracing in vivo, we investigate whether transdifferentiation of beta cells contributes to regeneration or metaplasia in pancreatitis. RIP-CreER;Z/AP mice were used to heritably tag beta cells in the adult pancreas. Injury by cerulein pancreatitis resulted in regeneration of normal tissue and metaplasia with formation of two distinct types of TC and mucinous lesions. Lineage tracing revealed that none of these MDL are of beta cell origin; nor do beta cells contribute to regeneration of normal acinar and ductal tissue, which indicates that the plasticity of differentiated pancreatic islet cells, suggested by earlier static and in vitro studies, plays no role in regeneration, metaplasia, and carcinogenesis in vivo.
Indexed as
Identifiers
What OpenQuestion holds
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.