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Editorial
. 2013 Oct;145(4):708-11.
doi: 10.1053/j.gastro.2013.08.023. Epub 2013 Aug 23.

The rapid rise in gastroesophageal junction tumors: is inflammation of the gastric cardia the underwater iceberg?

Michael Quante  1 , Julian A Abrams, Timothy C Wang
Affiliations
Editorial

The rapid rise in gastroesophageal junction tumors: is inflammation of the gastric cardia the underwater iceberg?

Michael Quante et al. Gastroenterology. 2013 Oct.
No abstract available

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Conflict of interest statement

Conflicts of interest

The authors disclose no conflicts.

Figures

Figure 1
Figure 1
In a proposed model of Barrett’s esophagus (BE), the proximal extension of original cardiac mucosa originates metaplasia in the esophagus. In obese patients, accelerated influx of immune cells and expression of cytokines, as well as an increased intra-abdominal pressure with an increased exposure of bile and gastric acid to the lower esophageal sphincter (LES) likely results in an altered microenvironment at the squa-mocolumnar junction (SCJ) that induce a lengthening of the cardiac mucosa through an expansion of adjacent cardiac glands.
See this image and copyright information in PMC

Comment on

References

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