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Detection of p53 Common Intron Polymorphisms in Patients with Gastritis Lesions from Iran

  • Sadeghi, Rouhallah Najjar (Research Center for Gastroenterology and Liver Diseases, Taleghani Hospital) ;
  • Damavand, Behzad (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Vahedi, Mohsen (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Mohebbi, Seyed Reza (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Zojazi, Homayon (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Molaei, Mahsa (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences) ;
  • Zali, Mohamad Reza (Research Center for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical sciences)
  • Published : 2013.01.31

Abstract

Background: p53 alterations have been implicated in the development of many cancers, such as gastric cancer, but there is no evidence of p53 intron alterations in gastritis lesions. The aim of this study was to investigate the p53 intron alterations in gastritis along with p53 and mismatch repair protein expression and microsatellite status. Materials and Methods: PCR-sequencing was conducted for introns 2-7 on DNA extracted from 97 paired samples of gastritis lesions and normal adjacent tissue. Abnormal accumulation of p53 and mismatch repair proteins was investigated using immunohistochemistry. In addition, microsatellite status was evaluated with reference to five mononucleotide markers. Results: Gastritis cases included 41 males and 56 females in the age range of 15-83 years, 87.6% being H.pylori positive. IVS2+38, IVS3ins16 and IVS7+72 were the most polymorphic sites. Their minor allele frequency values were as follows: 0.38, 0.21 and 0.06, respectively. Samples with GG genotype at IVS2+38 and CT at IVS7+72 had no insertion. Moreover, most of the stable samples (91.9 %) had a G allele at IVS2+38. All of the samples were IHC negative for p53 protein, microsatellite stable and expressed mismatch repair proteins. p53 alterations were prominent in the H. Pylori+ group, but without statistical significance. Conclusions: According to our results, some p53 polymorphisms such as IVS2+38, IVS3ins16 and IVS7+72, because of their correlations together or with microsatellite status may contribute to gastritis development. However, so far effects on p53 expression and function remain unclear. Therefore, a comprehensive survey is needed to delineate their biological significance.

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