ReviewCancer letters2009
Esophageal adenocarcinoma arising in Barrett esophagus.
Review in Cancer letters, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03813381 (The Impact of a Moderate CAlorie and Protein REstriction PROgram), which is not on this map. Cited by 25 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.
The Impact of a Moderate CAlorie and Protein REstriction PROgram (CARE-PRO) as an Efficient and Affordable Therapeutic Strategy in Patients With Barrett's Esophagus.
Who cites it
25 citing papers in PubMed, 78 citations in OpenAlex.
- Advances in gastrointestinal endoscopy: A comprehensive review of innovations in cancer diagnosis and management.World journal of gastrointestinal endoscopy · 2025Review
- Unveiling the intricacies: Insight into gastroesophageal reflux disease.World journal of gastroenterology · 2025Review
- The Association Between Gastroesophageal Reflux Disease and Non-Small Cell Lung Cancer: A Retrospective Case-Control Study.Gastroenterology research · 2022Article
- Alteration of protein expression and spliceosome pathway activity during Barrett's carcinogenesis.Journal of gastroenterology · 2021Article
- Krüppel-like Factor 5 Promotes Sonic Hedgehog Signaling and Neoplasia in Barrett's Esophagus and Esophageal Adenocarcinoma.Translational oncology · 2019Article
- Etiology, cancer stem cells and potential diagnostic biomarkers for esophageal cancer.Cancer letters · 2019Review
- Expression of Gastric Markers Is Associated with Malignant Potential of Nonampullary Duodenal Adenocarcinoma.Digestive diseases and sciences · 2018Article
- Role of nitric oxide in the pathogenesis of Barrett's-associated carcinogenesis.World journal of gastrointestinal pathophysiology · 2016Review
- Article
- Loss of glutathione peroxidase 7 promotes TNF-α-induced NF-κB activation in Barrett's carcinogenesis.Carcinogenesis · 2014Article
- Glutathione Peroxidase 7 Suppresses Bile Salt-Induced Expression of Pro-Inflammatory Cytokines in Barrett's Carcinogenesis.Journal of Cancer · 2014Article
- Targeting chemokine pathways in esophageal adenocarcinoma.Cell cycle (Georgetown, Tex.) · 2014Article
- Proinflammatory cytokines and bile acids upregulate ΔNp73 protein, an inhibitor of p53 and p73 tumor suppressors.PloS one · 2013Article
- ABL regulation by AXL promotes cisplatin resistance in esophageal cancer.Cancer research · 2013Article
- Risk of esophagus cancer in diabetes mellitus: a population-based case-control study in Taiwan.BMC gastroenterology · 2012Article
- Radiofrequency ablation for dysplasia in Barrett's esophagus restores β-catenin activation within esophageal progenitor cells.Digestive diseases and sciences · 2012Article
- Occurrence of multipolar mitoses and association with Aurora-A/-B kinases and p53 mutations in aneuploid esophageal carcinoma cells.BMC cell biology · 2011Article
- Widespread hypomethylation occurs early and synergizes with gene amplification during esophageal carcinogenesis.PLoS genetics · 2011Article
- Esophageal adenocarcinoma: treatment modalities in the era of targeted therapy.Digestive diseases and sciences · 2010Review
- The Axl receptor tyrosine kinase is an adverse prognostic factor and a therapeutic target in esophageal adenocarcinoma.Cancer biology & therapy · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The major risk factors for esophageal adenocarcinoma are gastroesophageal reflux disease (GERD) and Barrett esophagus, a squamous-to-columnar cell metaplasia that predisposes to malignancy. Adenocarcinomas in Barrett esophagus are thought to arise through a sequence of growth-promoting, genetic alterations that accumulate until the cells have acquired the physiologic hallmarks of cancer proposed by Hanahan and Weinberg. Moreover, GERD and Barrett esophagus are associated with chronic esophagitis, and inflammation is a well known risk factor for cancer formation. The cell that gives rise to Barrett metaplasia is not known. It has been proposed that the metaplasia may arise from a change in the differentiation pattern of stem cells that either reside in the esophagus or are recruited to the esophagus from the bone marrow. Alternatively, it is possible that Barrett metaplasia develops through the conversion of one differentiated cell type into another. Regardless of the cell of origin, Barrett metaplasia ultimately must be sustained by stem cells, which might be identified by intestinal stem cell markers. An emerging concept in tumor biology is that cancer stem cells are responsible for sustaining tumor growth. If Barrett cancers develop from Barrett stem cells, then a therapy targeted at those stem cells might prevent esophageal adenocarcinoma. This report reviews the risk factors for Barrett esophagus and esophageal adenocarcinoma, the mechanisms by which genetic alterations might contribute to carcinogenesis in Barrett esophagus, and the role of stem cells in the development of Barrett metaplasia and adenocarcinoma.
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.