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위장관 ; 헬리코박터 파일로리에 감염된 위 상피세포에서 DNA 이중나선절단 관찰
장영준 ( Young Jun Chang ),변상원 ( Sang Won Byun ),김형근 ( Hyung Keun Kim ),조영석 ( Young Seok Cho ),김성수 ( Sung Soo Kim ),김진일 ( Jin Il Kim ),김재광 ( Jae Kwang Kim ),정은선 ( Eun Sun Jung ) 대한소화기학회 2012 대한소화기학회지 Vol.60 No.2
Background/Aims: 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 γH2AX, 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 γH2AX 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. (Korean J Gastroenterol 2012;60:79-85)
김정호 ( Jeong Ho Kim ),김성수 ( Sung Soo Kim ),변상원 ( Sang Won Byun ),장영준 ( Young Jun Chang ),김진수 ( Jin Su Kim ),김재광 ( Jae Kwang Kim ),조항주 ( Hang Joo Cho ),임근우 ( Keun Woo Lim ),정은선 ( Eun Sun Jung ) 대한소화기학회 2010 대한소화기학회지 Vol.55 No.1
목적: DNA 이중사슬 절단은 DNA 손상의 한 형태로서 p53 돌연변이 등이 있는 세포에서 치유되지 않은 DSB가 핵 내에 축적될 경우 염색체 불안정을 유도하거나 혹은 암 발생 관련 유전자의 돌연변이 과정을 통해 암세포로 변환될 수 있다. 이에 이번 연구는 암 주위 정상, 선종 및 위암 조직에서 DNA 이중사슬 절단의 표지자인 53BP1과 γ-H2AX단백의 발현 양상을 관찰하였다. 대상 및 방법: 위절제술을 받았던 121예의 위암 환자와 내시경하 점막하 박리술을 받았던 51예의 위선종 환자를 대상으로 각각 tissue microarray를 만든 후 53BP1과 γ-H2AX 단백 각각에 대한 항체로 면역조직화학염색을 하여 발현 지수를 측정하였다. 결과: 53BP1과 γ-H2AX는 암 주위 정상 조직에 비해 위암 조직에서 발현율이 높았으나(p<0.01), 암 주위 정상 조직과 위선종 조직 간에 53BP1과 γ-H2AX 단백의 발현은 차이가 없었다. 위선종 조직에서 53BP1는 이형성 등급 I에 비해 II 및 III의 발현지수가 유의하게 높았다. 위암 환자에서 임상-병리학적 인자는 53BP1 및 γ-H2AX 단백의 발현과 상관관계가 없었다. 결론: 이상의 결과로 보아 DNA 이중사슬절단은 위암 발생과정에 관여하는 것으로 보이나 위선종 세포에서는 별다른 역할을 하지 않는 것으로 보인다. Background/Aims: DNA double strand break (DSB) is one of the critical types of DNA damage. When un-repaired DSB is accumulated in the nucleus of the cells having mutations in such genes as p53, it will lead to chromosomal instability and further more to mutation of tumor-activating genes resulting in tumorogenesis. Some of malignant cancers and its premalignant lesions were proven to have DSB in their nuclei. The aim of this study was to define the differences in expression of 53BP1 and γ-H2AX, the markers of DSB, among normal, gastric adenoma, and gastric adenocarcinoma tissues. Methods: Tissue microarray was made with the tissues taken from 121 patients who underwent gastrectomy for gastric adenocarcinoma, and 51 patients who underwent endoscopic mucosal resection for gastric adenoma. Immunochemical stain was performed for the marker of DSB, 53BP1 and γ-H2AX in the tissue microarray. The normal tissues were collected from histologically confirmed tissues with no cellular atypia obtained from the patients with gastric adenocarcinoma. Results: In gastric carcinoma cells, 53BP1 and γ-H2AX were highly expressed as compared to normal epithelial cells and gastric adenoma (p<0.01). There were no differences in the expression of 53BP1 and γ-H2AX between normal epithelium and gastric adenoma. The expression of 53BP1 in the adenoma with grade II and III atypism was more elevated than in those with grade I atypism. The expression of 53BP1 and γ-H2AX were not significantly different according to the clinicopathologic parameters in the patients with gastric adenocarcinoma. Conclusions: The DSB in DNA seems to be associated with the development of gastric adenocarcinoma, but does not affect the premalignant adenoma cells. (Korean J Gastroenterol 2010;55:19-25)