» Articles » PMID: 18703277

Esophageal Adenocarcinoma Arising in Barrett Esophagus

Overview
Journal Cancer Lett
Specialty Oncology
Date 2008 Aug 16
PMID 18703277
Citations 23
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Unveiling the intricacies: Insight into gastroesophageal reflux disease.

Wickramasinghe N, Devanarayana N World J Gastroenterol. 2025; 31(1):98479.

PMID: 39777237 PMC: 11684178. DOI: 10.3748/wjg.v31.i1.98479.


The Association Between Gastroesophageal Reflux Disease and Non-Small Cell Lung Cancer: A Retrospective Case-Control Study.

Amarnath S, Starr A, Chukkalore D, Elfiky A, Abureesh M, Aqsa A Gastroenterology Res. 2022; 15(4):173-179.

PMID: 36128185 PMC: 9451582. DOI: 10.14740/gr1537.


Alteration of protein expression and spliceosome pathway activity during Barrett's carcinogenesis.

Stingl C, Bureo Gonzalez A, Guzel C, Phoa K, Doukas M, Breimer G J Gastroenterol. 2021; 56(9):791-807.

PMID: 34227026 PMC: 8370908. DOI: 10.1007/s00535-021-01802-2.


Krüppel-like Factor 5 Promotes Sonic Hedgehog Signaling and Neoplasia in Barrett's Esophagus and Esophageal Adenocarcinoma.

Ng C, Ma K, Cheng Y, Miyashita T, Harmon J, Meltzer S Transl Oncol. 2019; 12(11):1432-1441.

PMID: 31401336 PMC: 6700477. DOI: 10.1016/j.tranon.2019.07.006.


Etiology, cancer stem cells and potential diagnostic biomarkers for esophageal cancer.

Liu K, Zhao T, Wang J, Chen Y, Zhang R, Lan X Cancer Lett. 2019; 458:21-28.

PMID: 31125642 PMC: 6597177. DOI: 10.1016/j.canlet.2019.05.018.


References
1.
Fitzgerald R, Abdalla S, Onwuegbusi B, Sirieix P, Saeed I, Burnham W . Inflammatory gradient in Barrett's oesophagus: implications for disease complications. Gut. 2002; 51(3):316-22. PMC: 1773354. DOI: 10.1136/gut.51.3.316. View

2.
Souza R, Shewmake K, Beer D, Cryer B, Spechler S . Selective inhibition of cyclooxygenase-2 suppresses growth and induces apoptosis in human esophageal adenocarcinoma cells. Cancer Res. 2000; 60(20):5767-72. View

3.
Wong N, Wilding J, Bartlett S, Liu Y, Warren B, Piris J . CDX1 is an important molecular mediator of Barrett's metaplasia. Proc Natl Acad Sci U S A. 2005; 102(21):7565-70. PMC: 1140438. DOI: 10.1073/pnas.0502031102. View

4.
Lagergren J, Bergstrom R, Lindgren A, Nyren O . Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med. 1999; 340(11):825-31. DOI: 10.1056/NEJM199903183401101. View

5.
Sommerer F, Vieth M, Markwarth A, Rohrich K, Vomschloss S, May A . Mutations of BRAF and KRAS2 in the development of Barrett's adenocarcinoma. Oncogene. 2004; 23(2):554-8. DOI: 10.1038/sj.onc.1207189. View