Barrett's esophagus

A molecular perspective

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Carcinogenesis in Barrett's esophagus involves the accumulation of DNA abnormalities that enable cells to 1) provide their own growth signals; 2) ignore growth-inhibitory signals; 3) avoid apoptosis; 4) replicate without limit; 5) sustain angiogenesis; and 6) invade and proliferate in unnatural locations. This report reviews recent publications describing molecular abnormalities in Barrett's esophagus that could lead to the acquisition of these key physiologic hallmarks of malignancy. Some recent reports suggest that the gastroesophageal reflux of acid and bile can activate molecular pathways that promote proliferation and interfere with apoptosis in Barrett's metaplastic cells. Inactivation of the p16 and p53 tumor suppressor genes through promoter methylation, gene mutation, or loss of heterozygosity appears to be important for carcinogenesis in Barrett's esophagus. Finally, this report discusses recent data regarding the role of the Cdx2 gene in the development of esophageal intestinal metaplasia.

Original languageEnglish (US)
Pages (from-to)177-181
Number of pages5
JournalCurrent Gastroenterology Reports
Volume7
Issue number3
StatePublished - Jun 2005

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Barrett Esophagus
Carcinogenesis
Apoptosis
Loss of Heterozygosity
Metaplasia
Growth
Gastroesophageal Reflux
Tumor Suppressor Genes
Bile Acids and Salts
Methylation
Genes
Mutation
DNA
Neoplasms

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Barrett's esophagus : A molecular perspective. / Spechler, Stuart Jon.

In: Current Gastroenterology Reports, Vol. 7, No. 3, 06.2005, p. 177-181.

Research output: Contribution to journalArticle

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