مقالات پذیرفته شده در پنجمین کنگره بین المللی زیست پزشکی
Helicobacter pylori cagL Polymorphism D58E59 in gastric cancer, peptic ulcer and gastritis in north of iran
Helicobacter pylori cagL Polymorphism D58E59 in gastric cancer, peptic ulcer and gastritis in north of iran
Mina Rezaee Cherati,1,*Hamid Reza Nouri ,2Seyed Jalal Zargar,3
1. Department of Cell & Molecular Biology, Kish International Campus, University of Tehran, Kish Island, Iran 2. Immunoregulation Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran 3. Department of Cell & Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran
Introduction: Gastric cancer and peptic ulcer are the most important gastrointestinal disorders in the world, including Iran, that H. pylori is an important risk factor in the development of these diseases. The cagL encoded by cagL genes and expressed in pathogenicity island (cagPAI) that this protein plays a fundamental role in binding to host cells. Hence, the aim of this study was to determine cagL gene polymorphisms in patients with H. pylori-positive and its relationship with peptic ulcer and gastric cancer in north of Iran.
Methods: This cross-sectional study was conducted on 100 patients with gastric cancer, peptic ulcer and gastritis, which was referred to the Shahid Beheshti and Ayatollah Rouhani hospitals of Babol in 2015.During endoscopy, gastric biopsies were taken and samples were saved in sterile conditions. DNA was extracted from the tissue samples and detection of H. pylori in biopsy samples were confirmed using PCR with glmM primers. The cagL gene was amplified by gene-specific primers and, then was confirmed by electrophoresis its. After that, DNA was extracted from agarose gel and DNA sequencing was done
Results: In the present study, 78.26% (18/23) of patients with gastric cancer, 46.6% (14/30) from gastritis and 74.4% (35/47) of peptic ulcer patients were positive for H. pylori which demonstrates the H. pylori infection in gastric cancer and peptic ulcer were significantly higher than gastritis (P<0.05). In total, 67 sample were investigated for presence of cagL. The gene positivity of the cagL was 71.6% (48/67) in patients were infected with H. pylori. Frequency of cagL in patients with gastric cancer and peptic ulcer compared to patients with gastritis was not significant (p>0.05). Study of cagL polymorphisms showed that people with peptic ulcers compared to patients with gastric cancer or gastritis patients had significantly amino acid aspartic acid (D) at position 58, while the amino acid asparagine (N) in patients with gastric cancer has been in this position. Polymorphism at position 60 also showed that people with peptic ulcer compared to other subjects significantly had the amino acid isoleucine (I) in this position. The presence of the amino acid glutamine (Q) and asparagine (N) at position 62 and 122 respectively increased (P <0.05) risk of gastric cancer and peptic ulcer development. Also, the amino acid valine (V) was significantly placed in 134 position in patients with gastric cancer compared to peptic ulcer or gastritis.
Conclusion: Infection with cagL positive H. pylori increases risk of serious gastro duodenal diseases such as peptic ulcers and gastric cancer. Also, presence of the amino acids: aspartic acid, isoleucine, glutamine and asparagine at position 58, 60, 62 and 122, respectively increase the risk of peptic ulcer development in H. pylori infected patients. However, presence of the amino acid asparagine, methionine, glutamine and asparagine at the same position alongside valine in position of 134 increase the risk of gastric cancer development