title: [DNA double strand breaks in gastric epithelium with Helicobacter pylori infection].
abstract: OBJECTIVE
  DNA double strand breaks (DSB) is one of the critical types of DNA damage. If unrepaired, DSB is accumulated in the nucleus of cells, the cells become apoptotic or transform to tumor by way of genomic instability. Some of malignant cancers and its premalignant lesions were proven to have DSB in their nuclei. There was no report that Helicobacter pylori (H. pylori), the gastric carcinogen, induce DNA DSB in gastric epithelium in vivo. The aim of this study was to investigate whether H. pylori induce DSB in the gastric epithelial cells of chronic gastritis.
  
  
  METHODS
  Immunohistochemical stains were performed for the DSB markers, phospho-53BP1 and gH2AX, in the gastric epithelium derived from 44 peptic ulcer disease patients before and after H. pylori eradication. DNA fragmentation assay was performed in the cell line to investigate the DNA damage by H. pylori infection.
  
  
  RESULTS
  The mean expression score of gH2AX was significantly higher in the H. pylori infected gastric epithelium as compared to the H. pylori eradicated gastric epithelium (8.8±5.5 vs. 6.2±5.3 respectively; p=0.008). The expression score of phospho-53BP1 between before and after eradication of H. pylori was not statistically different, but tended to be higher in H. pylori infection. DNA fragmentation was developed significantly more in the cell lines after infection with H. pylori.
  
  
  CONCLUSIONS
  DSB of DNA damage was typical feature of H. pylori infection in the gastric epithelium.
authors.affiliation: Department of Internal Medicine, The Catholic University of Korea Uijongbu St. Mary's Hospital, 271 Cheonbo-ro, Uijeongbu 480-717, Korea.
authors.forename: Young Jun
authors.initials: YJ
authors.lastname: Chang
authors.forename: Sang Won
authors.initials: SW
authors.lastname: Byun
authors.forename: Hyung Keun
authors.initials: HK
authors.lastname: Kim
authors.forename: Young Seok
authors.initials: YS
authors.lastname: Cho
authors.forename: Sung Soo
authors.initials: SS
authors.lastname: Kim
authors.forename: Jin Il
authors.initials: JI
authors.lastname: Kim
authors.forename: Jae Kwang
authors.initials: JK
authors.lastname: Kim
authors.forename: Eun Sun
authors.initials: ES
authors.lastname: Jung
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D045744:Cell Line, Tumor; D004247:DNA / Q000378:metabolism; D053903:DNA Breaks, Double-Stranded; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000378:metabolism*; D016480:Helicobacter pylori / Q000187:drug effects* / Q000472:pathogenicity; D006657:Histones / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000235:genetics / Q000473:pathology; D000071857:Tumor Suppressor p53-Binding Protein 1
chemical_list: D000900:Anti-Bacterial Agents; C468783:H2AX protein, human; D006657:Histones; D047908:Intracellular Signaling Peptides and Proteins; C498301:TP53BP1 protein, human; D000071857:Tumor Suppressor p53-Binding Protein 1; D004247:DNA