At 10 years, all abnormalities, except CDKN2A mutation and methylation, contributed to esophageal cancer risk significantly, ranging from loss of heterozygosity on chromosome 17 (relative risk [RR]=10.6; 95% confidence interval [CI] 5.2-21.3, P<0.001) to loss of heterozygosity on chromosome 9 (RR = 2.6; CI 1.1-6.0, P=0.03).
A panel of abnormalities including 17p loss of heterozygosity, DNA tetraploidy and aneuploidy, and 9p loss of heterozygosity was the best predictor of esophageal cancers (RR = 38.7; CI 10.8-138.5, P<0.001). These abnormalities inactivate tumor-suppressor genes critical for controlling cell growth, the researchers said.
Patients with no baseline abnormality had a 12% 10-year cumulative esophageal cancer incidence, whereas patients with 17p loss of heterozygosity, DNA content abnormalities, and 9p loss of heterozygosity had at least a 79.1% 10-year incidence.
On the other hand, among patients with zero, one, two, or three baseline panel abnormalities, there was a significant trend toward risk reduction among NSAID users compared with nonusers (P=0.01).