Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

---

Gastritis is one of the most common diseases of human stomach. Most of the time, it is asymptomatic and if not treated, can cause atrophy in gastric tissue. Gastritis seems to be a consequence of Helicobacter pylori infection. H. pylori can induce DNA double strand breaks in DNA and activates the error-prone DNA repair pathways that result in accumulation of mutations and genomic instability which may mediate gastric carcinogenesis. In this study, we assessed expression of CHEK2, DCLRE1C and XRCC4 genes which are involved in cell cycle arrest and DNA double strand break repair systems happening with Gastritis. One hundred and eighty biopsy specimens were collected from patients who were referred for endoscopic examination. 60 samples including 30 cases (H. pylori positive Moderate chronic gastritis) and 30 controls (H. pylori negative Mild chronic gastritis) were selected for RNA extraction. Later cDNA was synthesized and Real-Time PCR was used to assess expression of CHEK2, DCLRE1C, XRCC4 and B2M genes. CHEK2, DCLRE1C and XRCC genes showed 5.88, 6.7 and 3.4 up-regulation respectively in comparison to the controls. Increasing level of CHEK2, DCLRE1C and XRCC4 genes might be related to activation of these genes after H. pylori infection.

Keywords: Gastritis, Error-prone repair pathways, Double strand DNA breaks, H. Pylori, CHEK2, XRCC4, DCLRE1C

Full-Text [PDF 499 kb]   (694 Downloads)    

Add your comments about this article : Your username or Email:

---

---