ArticlePloS one2010
Malignant transformation of non-neoplastic Barrett's epithelial cells through well-defined genetic manipulations.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Trial
- In Barrett's esophagus patients and Barrett's cell lines, ursodeoxycholic acid increases antioxidant expression and prevents DNA damage by bile acids.American journal of physiology. Gastrointestinal and liver physiology · 2014Trial
- Article
- Context-dependent effects of CDKN2A and other 9p21 gene losses during the evolution of esophageal cancer.Nature cancer · 2025Article
- A human Barrett's esophagus organoid system reveals epithelial-mesenchymal plasticity induced by acid and bile salts.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- In Barrett's epithelial cells, weakly acidic bile salt solutions cause oxidative DNA damage with response and repair mediated by p38.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Acidic Bile Salts Induce Epithelial to Mesenchymal Transition via VEGF Signaling in Non-Neoplastic Barrett's Cells.Gastroenterology · 2019Article
- Centrosome amplification arises before neoplasia and increases upon p53 loss in tumorigenesis.The Journal of cell biology · 2018Article
- Authentication and characterisation of a new oesophageal adenocarcinoma cell line: MFD-1.Scientific reports · 2016Article
- NOD-Like Receptor Protein 3 Inflammasome Priming and Activation in Barrett's Epithelial Cells.Cellular and molecular gastroenterology and hepatology · 2016Article
- Mitochondrial STAT3 contributes to transformation of Barrett's epithelial cells that express oncogenic Ras in a p53-independent fashion.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Mechanisms of Barrett's oesophagus: intestinal differentiation, stem cells, and tissue models.Best practice & research. Clinical gastroenterology · 2015Review
- Autocrine VEGF signaling promotes proliferation of neoplastic Barrett's epithelial cells through a PLC-dependent pathway.Gastroenterology · 2014Article
- Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction.Cancer biology & therapy · 2013Review
- Targeting the intrinsic inflammatory pathway: honokiol exerts proapoptotic effects through STAT3 inhibition in transformed Barrett's cells.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Sex-dependent novelty response in neurexin-1α mutant mice.PloS one · 2012Article
- Deoxycholic acid causes DNA damage while inducing apoptotic resistance through NF-κB activation in benign Barrett's epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Cancer-related inflammation and Barrett's carcinogenesis: interleukin-6 and STAT3 mediate apoptotic resistance in transformed Barrett's cells.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundHuman Barrett's cancer cell lines have numerous, poorly-characterized genetic abnormalities and, consequently, those lines have limited utility as models for studying the early molecular events in carcinogenesis. Cell lines with well-defined genetic lesions that recapitulate various stages of neoplastic progression in Barrett's esophagus would be most useful for such studies. METHODOLOGY/PRINCIPAL
findingsTo develop such model cell lines, we started with telomerase-immortalized, non-neoplastic Barrett's epithelial (BAR-T) cells, which are spontaneously deficient in p16, and proceeded to knock down p53 using RNAi, to activate Ras by introducing oncogenic H-Ras(G12V), or both. BAR-T cells infected with either p53 RNAi or oncogenic H-Ras(G12V) alone maintained cell-to-cell contact inhibition and did not exhibit anchorage-independent growth in soft agar. In contrast, the combination of p53 RNAi knockdown with expression of oncogenic H-Ras(G12V) transformed the p16-deficient BAR-T cells, as evidenced by their loss of contact inhibition, by their formation of colonies in soft agar, and by their generation of tumors in immunodeficient mice. CONCLUSIONS/SIGNIFICANCE: Through these experiments, we have generated a number of transformed and non-transformed cell lines with well-characterized genetic abnormalities recapitulating various stages of carcinogenesis in Barrett's esophagus. These lines should be useful models for the study of carcinogenesis in Barrett's esophagus, and for testing the efficacy of chemopreventive and chemotherapeutic agents.
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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.