Azadeh Yazdani Cherati1, Yousef Yahyapour2, Mohammad Ranaee3, Mehdi Rajabnia2, Javad Shokri Shirvani4, Mahmoud Hajiahmadi5, Farzin Sadeghi6. 1. Students Research Committee, Babol University of Medical Sciences, Babol, Iran. 2. Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. 3. Department of Pathology, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran. 4. Department of Internal Medicine, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran. 5. Department of Community Medicine, Babol University of Medical Sciences, Babol, Iran. 6. Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Abstract
BACKGROUND: Helicobacter pylori (HP) infection is one of the hypothesized infectious etiologies of gastric cancer (GC) and other gastroduodenal diseases. It was suggested that other infectious agents, including oncogenic viruses, may increase the risk of gastroduodenal diseases. A number of reports regarding JC polyomavirus (JCPyV) have shown that JCPyV could be implicated in colorectal cancer and gastrointestinal carcinogenesis. OBJECTIVE: The current investigation aimed to investigate whether JCPyV could have any association with the pathogenesis of gastroduodenal diseases either alone or together with HP. METHODS: A total of 237 fresh or formalin-fixed and paraffin-embedded gastroduodenal samples were examined by quantitative real-time polymerase chain reaction targeting the JCPyV large tumor antigen (LTag) oncogene, and viral load was determined as viral copy number/cell. RESULTS: In total, 2 out of 237 samples (0.8%) were positive for JCPyV LTag DNA. One positive sample derived from diffuse-type gastric adenocarcinoma (6.8 × 10-3 copies/cell) and other JCPyV-positive sample obtained from a patient with gastritis (2.5 × 10-3 copies/cell) were recorded. Both JCPyV-positive samples were negative for HP infection. CONCLUSION: This study suggests no association between JCPyV infection and GC or other gastroduodenal diseases. The very low frequency of JCPyV LTag sequences in GC is an important aspect that weakens the hypothesis of the pathogenic role of JCPyV in gastric tumor induction.
BACKGROUND: Helicobacter pylori (HP) infection is one of the hypothesized infectious etiologies of gastric cancer (GC) and other gastroduodenal diseases. It was suggested that other infectious agents, including oncogenic viruses, may increase the risk of gastroduodenal diseases. A number of reports regarding JC polyomavirus (JCPyV) have shown that JCPyV could be implicated in colorectal cancer and gastrointestinal carcinogenesis. OBJECTIVE: The current investigation aimed to investigate whether JCPyV could have any association with the pathogenesis of gastroduodenal diseases either alone or together with HP. METHODS: A total of 237 fresh or formalin-fixed and paraffin-embedded gastroduodenal samples were examined by quantitative real-time polymerase chain reaction targeting the JCPyV large tumor antigen (LTag) oncogene, and viral load was determined as viral copy number/cell. RESULTS: In total, 2 out of 237 samples (0.8%) were positive for JCPyV LTag DNA. One positive sample derived from diffuse-type gastric adenocarcinoma (6.8 × 10-3 copies/cell) and other JCPyV-positive sample obtained from a patient with gastritis (2.5 × 10-3 copies/cell) were recorded. Both JCPyV-positive samples were negative for HP infection. CONCLUSION: This study suggests no association between JCPyV infection and GC or other gastroduodenal diseases. The very low frequency of JCPyV LTag sequences in GC is an important aspect that weakens the hypothesis of the pathogenic role of JCPyV in gastric tumor induction.
Authors: L Ricciardiello; L Laghi; P Ramamirtham; C L Chang; D K Chang; A E Randolph; C R Boland Journal: Gastroenterology Date: 2000-11 Impact factor: 22.682
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