Barrett's esophagus

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Intestinal metaplasia in Barrett's esophagus is a major risk factor for esophageal adenocarcinoma, a tumor whose incidence rate has more than tripled in the United States over the past 2 decades. Studies have identified a number of molecular abnormalities that may be involved in the progression from dysplasia to cancer in Barrett's esophagus, including altered expression of cadherins and catenins; inactivation of tumor-suppressor genes, such as p53, p21, p27, and p16; and increased activity of the enzymes cyclooxygenase- 2 and inducible nitric oxide synthase. Studies on the role of Helicobacter pylori in the pathogenesis of intestinal metaplasia at the gastroesophageal junction have yielded contradictory results. It appears, however, that gastric infection with strains of H. pylori containing a cagA gene associated with cytotoxin expression may protect against the development of dysplasia and adenocarcinoma in Barrett's esophagus. The role of ablation therapy for Barrett's esophagus remains controversial, largely because thermal and photochemical ablative techniques often leave loci of intestinal metaplasia behind.

Original languageEnglish (US)
Pages (from-to)352-358
Number of pages7
JournalCurrent Opinion in Gastroenterology
Volume15
Issue number4
DOIs
StatePublished - 1999

Fingerprint

Barrett Esophagus
Metaplasia
Helicobacter pylori
Adenocarcinoma
Catenins
Esophagogastric Junction
Cytotoxins
Nitric Oxide Synthase Type II
Cadherins
Cyclooxygenase 2
Tumor Suppressor Genes
Neoplasms
Stomach
Hot Temperature
Incidence
Enzymes
Infection
Genes
Therapeutics

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Barrett's esophagus. / Spechler, Stuart Jon.

In: Current Opinion in Gastroenterology, Vol. 15, No. 4, 1999, p. 352-358.

Research output: Contribution to journalArticle

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