New findings shed light on aspirin's effect in Barrett's esophagus

Last Updated: 2017-05-15

By David Douglas

NEW YORK (Reuters Health) - In esophageal squamous cells from patients with Barrett’s esophagus, aspirin prevents the expression of caudal-related homeobox transcription factor 2 (CDX2) that is usually induced by acid and bile salts, according to a new study.

“These findings elucidate molecular mechanisms that might explain why some (gastroesophageal reflux disease) patients develop Barrett’s oesophagus while others do not, and why aspirin appears to protect against the development of Barrett’s oesophagus in some recent case-control studies,” researchers write in Gut, online April 25.

Dr. Rhonda F. Souza of Baylor University Medical Center, in Dallas, Texas, and colleagues note that in their earlier work, they found esophageal squamous cells from patients with Barrett’s esophagus expressed the intestinal transcription factor CDX2 when exposed to acid and bile salts, while cells from people without Barrett’s did not.

CDX2, Dr. Souza explained in an email to Reuters Health, "is a target of NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells), another transcription factor and one that plays a major role in causing inflammation."

In the present study, "we found that acid and bile salts caused strong activation of NF-kappaB only in the esophageal squamous cells from patients with Barrett’s esophagus. This difference in NF-kappaB activation between esophageal squamous cells from patients with and without Barrett’s esophagus appears to account for their differences in CDX2 expression induced by acid and bile salts."

This, in turn, "might explain why only some patients with GERD (those in whom reflux causes strong activation of NF-kappaB) develop Barrett’s esophagus," Dr. Souza said. She added that the findings suggest “aspirin use might protect patients with GERD from developing Barrett’s esophagus."

Dr. Stephen J. Meltzer of The Johns Hopkins University School of Medicine in Baltimore, Maryland, who was not involved in the work, told Reuters Health by email, "This highly innovative study builds on extensive previous groundbreaking research from this group elucidating the cell biology of Barrett's neoplasia."

Dr. Meltzer, who is American Cancer Society Clinical Research Professor, concluded, "This particular paper provides a possible mechanistic explanation for the known cancer-preventive effects of aspirin in Barrett's patients."

SOURCE: http://bit.ly/2pPZAgE

Gut 2017.