ArticleThe American journal of gastroenterology2001
Predictors of progression in Barrett's esophagus II: baseline 17p (p53) loss of heterozygosity identifies a patient subset at increased risk for neoplastic progression.
Article in The American journal of gastroenterology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 2 of them syntheses 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
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
119 citing papers in PubMed, 2 syntheses or guidelines pooled it, 369 citations in OpenAlex.
- Aberrant p53 Immunostaining in Barrett's Esophagus Predicts Neoplastic Progression: Systematic Review and Meta-Analyses.Digestive diseases and sciences · 2019Pooled it
- Genetic Biomarkers of Barrett's Esophagus Susceptibility and Progression to Dysplasia and Cancer: A Systematic Review and Meta-Analysis.Digestive diseases and sciences · 2016Pooled it
- Review
- Context-dependent effects of CDKN2A and other 9p21 gene losses during the evolution of esophageal cancer.Nature cancer · 2025Article
- Review
- Protein adduction causes non-mutational inhibition of p53 tumor suppressor.Cell reports · 2023Article
- Utility of ancillary studies in the diagnosis and risk assessment of Barrett's esophagus and dysplasia.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Review
- Evolutionary dynamics in Barrett oesophagus: implications for surveillance, risk stratification and therapy.Nature reviews. Gastroenterology & hepatology · 2022Review
- Telomere shortening accelerates tumor initiation in the L2-IL1B mouse model of Barrett esophagus and emerges as a possible biomarker.Oncotarget · 2022Article
- Evolution and progression of Barrett's oesophagus to oesophageal cancer.Nature reviews. Cancer · 2021Review
- Alteration of protein expression and spliceosome pathway activity during Barrett's carcinogenesis.Journal of gastroenterology · 2021Article
- Somatic DNA copy number alterations in non-dysplastic Barrett's esophagus.Surgical endoscopy · 2021Article
- Massively Parallel Sequencing of Esophageal Brushings Enables an Aneuploidy-Based Classification of Patients With Barrett's Esophagus.Gastroenterology · 2021Article
- Endogenous aldehyde accumulation generates genotoxicity and exhaled biomarkers in esophageal adenocarcinoma.Nature communications · 2021Article
- Loss of SMAD4 Is Sufficient to Promote Tumorigenesis in a Model of Dysplastic Barrett's Esophagus.Cellular and molecular gastroenterology and hepatology · 2021Article
- Chaperones and Ubiquitin Ligases Balance Mutant p53 Protein Stability in Esophageal and Other Digestive Cancers.Cellular and molecular gastroenterology and hepatology · 2021Review
- Recurring Translocations in Barrett's Esophageal Adenocarcinoma.Frontiers in genetics · 2021Article
- Drivers of Esophageal Adenocarcinoma and Opportunities for Cancer Interception.Cellular and molecular gastroenterology and hepatology · 2021Article
- Barrett's Esophagus and Esophageal Adenocarcinoma Biomarkers.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020Article
- Towards screening Barrett's oesophagus: current guidelines, imaging modalities and future developments.Clinical journal of gastroenterology · 2020Review
59 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
objectivesMost patients with Barrett's esophagus do not progress to cancer, but those who do seem to have markedly increased survival when cancers are detected at an early stage. Most surveillance programs are based on histological assessment of dysplasia, but dysplasia is subject to observer variation and transient diagnoses of dysplasia increase the cost of medical care. We have previously validated flow cytometric increased 4N fractions and aneuploidy as predictors of progression to cancer in Barrett's esophagus. However, multiple somatic genetic lesions develop during neoplastic progression in Barrett's esophagus, and it is likely that a panel of objective biomarkers will be required to manage the cancer risk optimally.
methodsWe prospectively evaluated endoscopic biopsies from 325 patients with Barrett's esophagus, 269 of whom had one or more follow-up endoscopies, by a robust platform for loss of heterozygosity (LOH) analysis, using baseline 17p (p53) LOH as a predictor and increased 4N, aneuploidy, high-grade dysplasia, and esophageal adenocarcinoma as outcomes.
resultsThe prevalence of 17p (p53) LOH at baseline increased from 6% in negative for dysplasia to 57% in high-grade dysplasia (p < 0.001). Patients with 17p (p53) LOH had increased rates of progression to cancer (relative risk [RR] = 16, p < 0.001), high-grade dysplasia (RR = 3.6, p = 0.02), increased 4N (RR = 6.1, p < 0.001), and aneuploidy (RR = 7.5, p < 0.001).
conclusionsPatients with 17p (p53) LOH are at increased risk for progression to esophageal adenocarcinoma as well as high-grade dysplasia, increased 4N, and aneuploidy. 17p (p53) LOH is a predictor of progression in Barrett's esophagus that can be combined with a panel of other validated biomarkers for risk assessment as well as intermediate endpoints in prevention trials.
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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.