Employing a Helicobacter species-specific 16S rDNA PCR assay com

Employing a Helicobacter species-specific 16S rDNA PCR assay combined with pyrosequencing analysis, Grahn et al. detected the presence of Helicobacter DNA sequences in 21 of 77 (27%) CRC biopsy specimens (91). No nonneoplastic colorectal tissues were examined in the study because the authors did not have access to normal colorectal biopsy specimens according to the authors. However, in a different study using the same techniques, the researchers

were able to detect H. pylori DNA in 5 of 19 colon samples biopsied from 3 p38 MAPK inhibitor patients with microscopic colitis. No Inhibitors,research,lifescience,medical H. pylori DNA was detected in 12 rectal biopsies that were histologically normal (92). Although the exact route of H. pylori transmission has not been fully understood, person-to-person transmission via either oral-to-oral or fecal-to-oral route is most common. Since H. pylori organisms are shed in stools from infected individuals (93-95), it is not surprising that the organisms, which may just simply pass through the Inhibitors,research,lifescience,medical intestinal tract with digested contents, can be detected in colonic tissue samples. It should also be noted that H. pylori-associated gastric cancer is known to be the consequence of chronic active gastritis that leads to mucosal atrophy, intestinal metaplasia and dysplasia. However, there have been no reports of

chronic or active colitis resulted from direct H. pylori Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical infection in the colon. Based on our experience, the colonic mucosa in patients with H. pylori gastritis shows normal histology unless other medical conditions are present. Thus, simply identifying H. pylori organisms in colorectal tumor samples does not prove a causal relationship. Conclusions While the

etiopathogenetic role of H. pylori in gastric cancer Inhibitors,research,lifescience,medical is well-established, its role in colorectal tumorigenesis remains controversial. H. pylori infection of the stomach may promote colorectal tumorigenesis indirectly in a variety of ways such as modulating intestinal microflora, enhancing cytokine production and increasing gastrin secretion. These effects may be more pronounced Metalloexopeptidase when infected by more virulent H. pylori strains. Detection of H. pylori antigens and/or DNA in colonic tissue samples does not necessarily mean colonic colonization by the organisms, and should not be viewed as direct evidence of causal association with colorectal tumorigenesis. Acknowledgements Disclosure: The authors declare no conflict of interest.
Improved outcomes after curative resection for rectal cancer have been driven in part by total mesorectal excision (TME) and the introduction of neoadjuvant chemoradiation. An equally important consideration in optimizing prognosis is accurate pathological staging, which is highly dependent on accurate assessment of lymph node status after TME. The use of neoadjuvant treatment impacts lymph node harvests and affects pathologic staging.

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