ArticleThe American journal of pathology1998
Genetic alterations in Barrett esophagus and adenocarcinomas of the esophagus and esophagogastric junction region.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.
- Pooled it
- Correlation of histology with biomarker status after photodynamic therapy in Barrett esophagus.Cancer · 2008Trial
- Associations Between Non-Genetic Risk Factors and DNA Methylation Alterations in Barrett's Esophagus and Its Progression to Esophageal Adenocarcinoma.International journal of molecular sciences · 2025Review
- Review
- The Role of the Transforming Growth Factor-β Signaling Pathway in Gastrointestinal Cancers.Biomolecules · 2023Review
- SMAD Proteins in TGF-β Signalling Pathway in Cancer: Regulatory Mechanisms and Clinical Applications.Diagnostics (Basel, Switzerland) · 2023Review
- TGF-β Signaling in Liver, Pancreas, and Gastrointestinal Diseases and Cancer.Gastroenterology · 2021Review
- Molecular Evolution of Metaplasia to Adenocarcinoma in the Esophagus.Digestive diseases and sciences · 2018Review
- Epstein-Barr virus and mismatch repair deficiency status differ between oesophageal and gastric cancer: A large multi-centre study.European journal of cancer (Oxford, England : 1990) · 2018Article
- Pattern of p53 protein expression is predictive for survival in chemoradiotherapy-naive esophageal adenocarcinoma.Oncotarget · 2017Article
- Higher prevalence of colon polyps in patients with Barrett's esophagus: a case-control study.Gastroenterology report · 2014Article
- Transformation of benign Barrett's epithelium by repeated acid and bile exposure over 65 weeks: a novel in vitro model.International journal of cancer · 2011Article
- Genome-wide catalogue of chromosomal aberrations in barrett's esophagus and esophageal adenocarcinoma: a high-density single nucleotide polymorphism array analysis.Cancer prevention research (Philadelphia, Pa.) · 2010Article
- Loss of heterozygosity at thymidylate synthase locus in Barrett's metaplasia, dysplasia, and carcinoma sequences.BMC cancer · 2009Article
- Utility of biomarkers in prediction of response to ablative therapy in Barrett's esophagus.Gastroenterology · 2008Article
- Article
- TP53 gene mutations are rare in nondysplastic Barrett's esophagus.Digestive diseases and sciences · 2006Article
- Microsatellite instability in gastrointestinal tract cancers: a brief update.Surgery today · 2005Review
- The CHEK2(*)1100delC mutation has no major contribution in oesophageal carcinogenesis.British journal of cancer · 2004Article
- Characterisation of p53 status at the gene, chromosomal and protein levels in oesophageal adenocarcinoma.British journal of cancer · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of esophageal adenocarcinoma has increased markedly in the past two decades, but the genetic alterations in this cancer and its precursor, Barrett mucosa, have not been characterized extensively. DNA replication errors and allelic losses of chromosomes 17p, 18q, and 5q were studied in 36 resected adenocarcinomas arising in the esophagus and esophagogastric junction, 56 Barrett adenocarcinomas, and 11 dysplasias in Barrett esophagus. The results were compared with clinical and pathological characteristics, including patient survival. Replication error positive cancer was rare (5.4%) in esophageal adenocarcinomas and was not found in Barrett mucosa. There was an increase in the prevalence of chromosomal losses in the Barrett mucosa-columnar dysplasia-adenocarcinoma sequence: 17p loss occurred in 14% of Barrett mucosae, 42% of low-grade dysplasias, 79% of high-grade dysplasias, and 75% of adenocarcinomas, respectively; loss of 18q in 32%, 42%, 73%, and 69%; and loss of 5q in 10%, 21%, 27%, and 46%. Clinical stage was a very strong prognostic factor for survival, and adenocarcinomas with allelic loss of both 17p and 18q had worse survival than cancers with no or one allelic loss (P = 0.002). Our results indicate that accumulation of genetic alterations follows the dysplasia-adenocarcinoma sequence in the esophagus and that losses of 18q and 17p occur earlier than 5q loss. Allelic loss of both 17p and 18q in esophageal adenocarcinoma identifies patients with poor prognosis.
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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.