title: Detection of p53 common intron polymorphisms in patients with gastritis lesions from Iran.
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.
  
  
  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 HP+ 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.
authors.affiliation: Research Center for Gastroenterology and Liver Diseases, Taleghani Hospital, Shahid Beheshti University of Medical sciences, Tehran, Iran. najjarsadeghi@yahoo.com
authors.forename: Rouhallah
authors.initials: R
authors.lastname: Najjar Sadeghi
authors.forename: Behzad
authors.initials: B
authors.lastname: Damavand
authors.forename: Mohsen
authors.initials: M
authors.lastname: Vahedi
authors.forename: Seyed Reza
authors.initials: SR
authors.lastname: Mohebbi
authors.forename: Homayon
authors.initials: H
authors.lastname: Zojazi
authors.forename: Mahsa
authors.initials: M
authors.lastname: Molaei
authors.forename: Mohamad Reza
authors.initials: MR
authors.lastname: Zali
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D004268:DNA-Binding Proteins / Q000378:metabolism; D005260:Female; D005756:Gastritis / Q000235:genetics* / Q000382:microbiology; D005787:Gene Frequency; D016481:Helicobacter Infections / Q000382:microbiology; D016480:Helicobacter pylori; D006801:Humans; D007438:Introns; D007492:Iran; D008297:Male; D053842:Microsatellite Instability; D008875:Middle Aged; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein / Q000378:metabolism; D009687:Nuclear Proteins / Q000378:metabolism; D011110:Polymorphism, Genetic; D017422:Sequence Analysis, DNA; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D055815:Young Adult
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D004268:DNA-Binding Proteins; C094443:G-T mismatch-binding protein; C501486:MLH1 protein, human; D009687:Nuclear Proteins; D016159:Tumor Suppressor Protein p53; C497172:MSH2 protein, human; D000070957:MutL Protein Homolog 1; D051718:MutS Homolog 2 Protein