The strongest protective effect was seen among participants with multiple genetic abnormalities, with NSAID nonusers having an observed 10-year risk of 79%, compared with 30% for NSAID users (P<0.001).
The cluster of 17p loss of heterozygosity, 9p LOH, and DNA content abnormalities provided better esophageal adeonocarcinoma risk prediction than any single TP53, CDKN2A, or DNA content lesion alone, the researchers said.
Furthermore, they added, these results show a protective association between NSAID use and progression to esophageal cancer, particularly among those with multiple high-risk somatic genetic abnormalities.
It is hypothesized from experimental model systems and observational studies, that aspirin(Drug information on aspirin) and other NSAIDS inhibit cyclooxygenase 2 (Cox-2), increase apoptosis, decrease inflammation, decrease proliferation, and inhibit angiotenesis, Dr. Reid said.
