The incidence of AC in BE is low, confirming recent data from the literature reporting an overestimation of cancer risk in these patients. In our patient cohort, surveillance involved a large expenditure of effort but did not prevent any cancer deaths. The benefit of surveillance remains uncertain.

The prevalence of colorectal adenomatous polyps varies widely from country to country. Among asymptomatic, average-risk patients, adenoma prevalence averages approximately 10% in sigmoidoscopy studies and more than 25% in colonoscopy studies, whereas the prevalence of colorectal cancer among these patients is less than 1%. These data may change in the future due to the advent of new technological approaches and, in particular, chromo- and magnifying endoscopy as well as confocal laser endoscopy. The cumulative incidence of new adenomas within 3 years after normal endoscopy averages about 7% by flexible sigmoidoscopy and 27% by colonoscopy. As far as risk factors for colorectal adenomas are concerned, several data are now available on the potential role of various diet items. Tobacco smoking may be important in the early stages of adenoma formation, but not necessarily in the later stages. Alcohol consumption elevates the risk of adenomatous colorectal polyps and this seems increased by ADH3 polymorphism. Another gene-environment relationship of interest in colorectal tumorigenesis may be based on folate's effects on K-ras mutations.

Our study showed a statistically significant effect of antioxidant supplementation on adenoma recurrence. Further clinical trials are needed to address the role of antioxidants in subgroups of subjects at increased risk for colorectal cancer.

No abstract

Inflammation and oxidative stress play a crucial role in the development of colorectal cancer (CRC) and interference with these mechanisms represents a strategy in CRC chemoprevention. Allopurinol, a safe molecular scavenger largely used as antigout agent, has been shown to increase survival of patients with advanced CRC and to reduce CRC incidence in long-term gout users in epidemiologic studies. We conducted a randomized, double-blind, placebo-controlled preoperative trial in subjects with colorectal adenomatous polyps to assess the activity of allopurinol on biomarkers of colorectal carcinogenesis.After complete colonoscopy and biopsy of the index polyp, 73 subjects with colorectal adenomas were assigned to either placebo or one of two doses of allopurinol (100 mg or 300 mg) and treated for four weeks before polyp removal. Change of Ki-67 labeling index in adenomatous tissue was the primary endpoint. Secondary endpoints were the immunohistochemical (IHC) expression of NF-kB, b-catenin, topoisomerase-II-a, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) in adenomatous polyps and normal adjacent colonic tissue.Compared with placebo, Ki-67 levels were not significantly modulated by allopurinol, whereas b-catenin and NF-kB expression levels decreased significantly in adenomatous tissue, with a mean change from baseline of À10.6%, 95% confidence interval (CI), À20.5 to À0.7, and À8.1%, 95% CI, À22.7 to 6.5, respectively. NF-kB also decreased significantly in normal adjacent tissue (À16.4%; 95% CI, À29.0 to À3.8).No dose-response relationship was noted, except for NF-kB expression in normal tissue.Allopurinol can inhibit biomarkers of oxidative activation in colon adenomatous polyps and normal adjacent tissue. Further studies should define its potential chemopreventive activity. Cancer Prev Res; 6(2); 74-81. Ó2012 AACR.