Background and aims: The aim of this study was to detect Helicobacter pylori (H. pylori) in colorectal cancer tissue specimens and relate the possible role of this microorganism in the etiology of colorectal cancer.
Patients and methods: From February 2002 to April 2003 83 CRC patients (55 male, 28 female) and 40 control patients (19 male, 21 female) entered the prospective study. The biopsy samples of CRC tissue and normal mucosa were obtained during open surgery on CRC patients. In the control patients biopsy samples were taken during colonoscopy. Pathology confirmed adenocarcinoma in all the CRC patients. The existence of genetic material of H. pylori was determined by detection of the ureA gene by nested PCR. K-ras PCR was also performed on all patients.
Results: H. pylori PCR was positive in 1 case (1.2%) of CRC in the tumour tissue and in all 5 samples (6.0%) of the normal colonic mucosa in the cancer patients. The control patients were PCR positive to H. pylori in 13 samples (32.5%). According to Chi-square test, there is no statistical correlation between H. pylori infection and CRC (x2 = 2.9395; p > 0.05) but there is a significant prevalence of H. pylori infection in controls compared to CRC (x2 = 15.5625; p < 0.01). The K-ras PCR showed gene mutations in 19 tumour tissues of CRC (31.6%) and in 2 cases (3.4%) of normal colonic mucosa of CRC patients . In controls K-ras PCR showed one gene mutation (3.0%). There is a significant statistical correlation between K-ras mutation and CRC (x2 = 16.0694; p < 0.01).
Conclusion: Our established PCR for H. pylori is feasible for CRC tissue as well. However, H. pylori is not considered to play an important role in the pathogenesis of CRC. The identification of K-ras mutations in routine PCR analysis correlates with the presence of CRC.