Nonsteroidal anti-inflammatory drugs may give some protection against esophageal adenocarcinoma developing from its premalignant state, Barrett’s esophagus.
Genetic abnormalities are common in many human cancers and their precursors, including esophageal adenocarcinoma and Barrett’s esophagus. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have been proposed as possible chemoprevention against esophageal adenocarcinoma and Barrett’s esophagus.
A study of 243 patients with Barrett’s esophagus followed up for 10 years by Patricia Galipeau and colleagues from the Fred Hutchinson Cancer Research Center, Seattle looked at various genetic changes, including specific mutations and variations in the total amount of DNA present. They assessed whether each genetic abnormality was associated with the risk of developing esophageal adenocarcinoma, and whether the risk was altered in patients who had taken aspirin or other NSAIDs.
The researchers found that over 10 y, all abnormalities, except two, contributed significantly to the risk of developing esophageal adenocarcinoma. A panel of genetic abnormalities was the best predictor of developing esophageal adenocarcinoma; over 10 years patients with no baseline abnormality had a 12% cumulative incidence of esophageal adenocarcinoma, whereas patients with the full panel of genetic abnormalities had a 79% incidence. In patients with none, one, two, or three baseline genetic abnormalities, the risk of developing esophageal adenocarcinoma was significantly reduced among users of NSAIDs compared to nonusers, with the strongest protective effect being seen in participants with multiple genetic abnormalities.
These findings may have implications for the treatment of patient with Barrett’s esophagus, but especially since this is an observational study, and not a randomised trial, it will need to be confirmed in other groups of patients.
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Citation: Galipeau PC, Li X, Blount PL, Maley CC, Sanchez CA, et al. (2007) NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma. PLoS Med 4(2): e67.
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Patricia Galipeau
Fred Hutchinson Cancer Research Center
Human Biology
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