RESUMO
Background: Around half of the global population is chronically infected with the stomach bacterium Helicobacter pylori, making it one of the most common chronic infections worldwide. H. pylori induces the production of reactive oxygen species, DNA damage, and accelerates the degradation of the tumor suppressor protein p53, which may lead to cancer development. In this study, we investigated the relationship between H. pylori infection and the expression of p53 in gastric mucosa in a group of patients from Jordan. Methods: In this retrospective case-control study, the epithelium of gastric glands in subjects chronically infected with H. pylori was examined for the expression of p53. Paraffin-embedded gastric biopsy samples from the archives for 50 Jordanian patients diagnosed with chronic H. pylori infection and 25 samples free of H. pylori infection and any other gastric abnormalities were selected. Samples were analyzed for the presence of H. pylori as well as p53 expression levels in the mucosa and submucosa by immunohistochemical analyses and Western blotting. Results: H. pylori was detected in the gastric tissues of infected individuals (n = 50); whereas, no H. pylori infection was detected in uninfected healthy individuals (n = 25) using immunohistochemistry. In contrast to the noninfected samples of gastric mucosa, no nuclear p53 expression was detected in the infected samples using immunohistochemistry. In addition, the levels of p53 in H. pylori-positive samples detected by Western blotting were significantly lower than those in the negative individuals. Conclusion: Our data reveal that p53 protein expression decreased in gastric mucosa of patients infected with H. pylori. The loss of this tumor suppressor may play a role in the increased risk for tumor initiation associated with H. pylori carriage.
RESUMO
BACKGROUND: Endometrial and cervical carcinomas are the most common gynecologic malignancies in Western world and many countries. The human papillomavirus (HPV) high-risk genotypes are associated with cervical carcinoma (CC). Chlamydia trachomatis (C. trachomatis), the most common sexually transmitted bacterial infection worldwide, considered a cofactor for HPV infection and CC. Information on HPV infection rate and type distribution among Jordanian women having CC is currently limited and unavailable among those with endometrial carcinoma. Therefore, the present study aimed to provide an updated estimate on HPV infection rate and its high-risk genotypes' distribution among Jordanian women by comparing data from invasive cervical carcinoma (ICC) to normal cervical tissues. Similarly, assessment of HPV infection rate was extended to the endometrial tissues. C. trachomatis infection was investigated as well to explore its possibility as HPV cofactor for induction of such carcinomas. METHODS: Total DNA was extracted from 144 formaldehyde-fixed paraffin-embedded cervical and endometrial tissue, equally divided between age-matched control and carcinoma cases. Polymerase chain reaction (PCR) was used for general detection of HPV-DNA, high risk HPV-16 and 18 genotypes and C. trachomatis DNA using specific primers. RESULTS: HPV infection was detected in 91.7% and 61.1% of cervical cancer patients and controls, respectively. Likewise, it was higher among cases (47.2%) than controls (13.8%) in endometrial biopsies. Significantly higher HPV infection rates were found among ICC and endometrial control biopsies of women >50 years. Out of 33 HPV positive ICC cases, single HPV-16 infections were detected in 69.7% compared to HPV-18 (15.2%), while HPV-16/18 co-infections were only found in three (9%) samples. C. trachomatis was not detected in all studied groups. CONCLUSION: The present study has successfully provided an updated estimate on HPV infection rate among Jordanian women with and without ICC and endometrial carcinoma. In addition, a lack of co-infection was observed between HPV and C. trachomatis in both cancer types.