pylori organisms, especially the more virulent strains, to have a greater chance to successfully establish infection in these patients. If infection by cagA-positive H. pylori strains does in fact precede and contribute to the development of CRC, the underlying mechanisms remains elusive. It has been shown that infection by cagA-positive strains is associated with higher levels of gastrin than that by cagA-negative strains (82,83). Overproduction of IL-8, which is known to be a growth factor for human colon carcinoma cells (8-11), may

also be implicated (81,84,85). In addition, infection with cagA-positive H. pylori strains is associated Inhibitors,research,lifescience,medical with an increased likelihood of developing atrophic gastritis (86-88), which would be expected to sustain a more drastic disruption of the gastric acid http://www.selleckchem.com/MEK.html barrier function to allow for

an abnormal bacterial colonization in the lower intestinal tract as discussed above. Chronic inflammation secondary to direct H. pylori colonization in the colon Chronic mucosal inflammation is believed to be a predisposing Inhibitors,research,lifescience,medical factor for CRC development, as evidenced by inflammatory bowel disease. Given H. pylori’s well-established proinflammatory and carcinogenic effect in the stomach, a “chronic inflammation → dysplasia → neoplasia” sequence, similar to that for inflammatory bowel disease, may occur Inhibitors,research,lifescience,medical in the colon initiated by direct H. pylori colonization. In this regard, Kapetanakis et al. reported detection of H. pylori organisms in malignant tissues from 34 of 41 (82.9%) CRC patients by cresyl violet staining and immunohistochemistry (32). Using the same staining methods, the authors recently extended their study to 50 patients with CRC and 25 patients with colonic polyps and found that H. pylori organisms were present in 84% CRC tissues and Inhibitors,research,lifescience,medical 64% polyps (1). It is unclear, however, whether the authors have also included nonneoplastic colonic tissues for comparison Inhibitors,research,lifescience,medical in their studies, where the organisms were located in the

tissues, and what staining characteristics they have observed for the organisms. Soylu et al. examined 51 colonic polyps (39 tubular adenomas, 3 tubulovillous adenomas, 5 villous adenomas, and 4 adenocarcinomas) Resminostat by immunohistochemistry and demonstrated positive staining in 11 (21.6%) polyps. In 10 (90.9%) polyps, however, the positive staining was interpreted as equivocal and appeared nonspecific (89). Again, no nonneoplastic colonic mucosa was included for comparison. In the study by Jones et al., a total of 176 colorectal specimens (normal 58, adenoma 59, adenocarcinoma 59) were examined by H. pylori immunohistochemistry. Positive staining was seen in 1 (1.7%) normal sample, 9 (15.3%) adenomas, and 10 (16.9%) adenocarcinomas (90). However, all the positive cases showed granular and dot-like staining patterns; none of the positive cases demonstrated an unequivocal spiral form of H. pylori organisms as typically seen in the stomach.