中华消化杂志
中華消化雜誌
중화소화잡지
Chinese Journal of Digestion
2001年
1期
11-14
,共4页
何兴祥%王家%吴捷莉%袁顺玉%艾莉
何興祥%王傢%吳捷莉%袁順玉%艾莉
하흥상%왕가%오첩리%원순옥%애리
端粒%DNA倍性%肠化%胃癌
耑粒%DNA倍性%腸化%胃癌
단립%DNA배성%장화%위암
目的 分析不同病变胃黏膜细胞内端粒长度的差异,以及细胞内DNA含量,探讨端粒行为异常、细胞内DNA含量与胃黏膜癌变的关系。方法 应用Southern杂交分析细胞内端粒长度,应用流式细胞术测定细胞内DNA含量。结果 在172例胃镜活检标本中,正常胃黏膜,慢性浅表性胃炎(CSG),伴0、1、2度肠化的慢性萎缩性胃炎(CAG)和胃癌组织的端粒长度,分别是(10.42±0.2)kb,(9.86±0.4)kb,(9.78±1.2)kb、(8.64±1.0)kb、(6.22±1.2)kb和(5.86±2.6)kb。45例胃癌手术标本结果 相似。流式细胞术分析细胞内DNA含量,在胃镜活检标本中,正常胃黏膜,CSG,伴0、1、2度肠化的CAG和胃癌组织的异倍体DNA检出率分别为0、0、0、10.00%、12.50%6和33.33%6。45例胃癌手术切除标本结果 相似。异倍体细胞内端粒长度明显短于二倍体细胞,异倍体细胞中端粒长度与DNA指数呈负相关(r=-0.91,P<0.01),即端粒越短,DNA指数越高。结论 端粒长度从正常胃黏膜、不同程度肠化胃黏膜到癌变胃黏膜逐渐缩短。在正常胃黏膜和CSG中未检出异倍体DNA,从1度、2度肠化到癌变胃黏膜异倍体DNA检出率逐渐增高,而在异倍体细胞中端粒长度和DNA指数呈负相关。推测,可能存在端粒愈短,DNA扩增愈活跃。端粒缩短伴DNA指数增加可能是胃癌发生的先兆。
目的 分析不同病變胃黏膜細胞內耑粒長度的差異,以及細胞內DNA含量,探討耑粒行為異常、細胞內DNA含量與胃黏膜癌變的關繫。方法 應用Southern雜交分析細胞內耑粒長度,應用流式細胞術測定細胞內DNA含量。結果 在172例胃鏡活檢標本中,正常胃黏膜,慢性淺錶性胃炎(CSG),伴0、1、2度腸化的慢性萎縮性胃炎(CAG)和胃癌組織的耑粒長度,分彆是(10.42±0.2)kb,(9.86±0.4)kb,(9.78±1.2)kb、(8.64±1.0)kb、(6.22±1.2)kb和(5.86±2.6)kb。45例胃癌手術標本結果 相似。流式細胞術分析細胞內DNA含量,在胃鏡活檢標本中,正常胃黏膜,CSG,伴0、1、2度腸化的CAG和胃癌組織的異倍體DNA檢齣率分彆為0、0、0、10.00%、12.50%6和33.33%6。45例胃癌手術切除標本結果 相似。異倍體細胞內耑粒長度明顯短于二倍體細胞,異倍體細胞中耑粒長度與DNA指數呈負相關(r=-0.91,P<0.01),即耑粒越短,DNA指數越高。結論 耑粒長度從正常胃黏膜、不同程度腸化胃黏膜到癌變胃黏膜逐漸縮短。在正常胃黏膜和CSG中未檢齣異倍體DNA,從1度、2度腸化到癌變胃黏膜異倍體DNA檢齣率逐漸增高,而在異倍體細胞中耑粒長度和DNA指數呈負相關。推測,可能存在耑粒愈短,DNA擴增愈活躍。耑粒縮短伴DNA指數增加可能是胃癌髮生的先兆。
목적 분석불동병변위점막세포내단립장도적차이,이급세포내DNA함량,탐토단립행위이상、세포내DNA함량여위점막암변적관계。방법 응용Southern잡교분석세포내단립장도,응용류식세포술측정세포내DNA함량。결과 재172례위경활검표본중,정상위점막,만성천표성위염(CSG),반0、1、2도장화적만성위축성위염(CAG)화위암조직적단립장도,분별시(10.42±0.2)kb,(9.86±0.4)kb,(9.78±1.2)kb、(8.64±1.0)kb、(6.22±1.2)kb화(5.86±2.6)kb。45례위암수술표본결과 상사。류식세포술분석세포내DNA함량,재위경활검표본중,정상위점막,CSG,반0、1、2도장화적CAG화위암조직적이배체DNA검출솔분별위0、0、0、10.00%、12.50%6화33.33%6。45례위암수술절제표본결과 상사。이배체세포내단립장도명현단우이배체세포,이배체세포중단립장도여DNA지수정부상관(r=-0.91,P<0.01),즉단립월단,DNA지수월고。결론 단립장도종정상위점막、불동정도장화위점막도암변위점막축점축단。재정상위점막화CSG중미검출이배체DNA,종1도、2도장화도암변위점막이배체DNA검출솔축점증고,이재이배체세포중단립장도화DNA지수정부상관。추측,가능존재단립유단,DNA확증유활약。단립축단반DNA지수증가가능시위암발생적선조。
Objective To investigate telomere length and cellular DNA content in different gastric lesion mucosa, and their relation with gastric mucosal carcinogenesis. Methods Telomere length were determined by southern hybridization. Cellular DNA content was detected by flow cytometry. Results Telomere length in intestinal metaplasia (IM) grade 2 was significantly shorter than that in normal gastric, IM grade 0 or grade 1. Telemere length of gastric carcinoma cells was the shortest in all of the biopsy specimens. Telomere length ratio in patients of corresponding surrounding nontumorous tissues with IM grade 2 was the largest in 45 resected gastric carcinoma. In flow cytometry, The aneuploid of gastric carcinoma (n= 18), chronic atrophic gastritis (CAG) contained IM grade 2 (n= 8), grade 1 (n= 40), grade 0 (n= 20), chronic superficial gastritis (CSG n=46) and normal gastric mucosa (n = 10) was 33.3%, 12.5%, 10.0%, 0.0% ,0.0% and 0.0%, rspectively, in all of the biopsy specimens. In 45 resected gastric carcinoma specimens, Telomere length of 18 aneuploid was significantly shorter than that of 27 diploid. Furthermore reverse correlation was observed between telomere length and the DNA index in 18 aneuploid. Conclusions Telomere length were shortened as normal mucosa changed into intestinal metaplasia and more into gastric cancer. The normal and CSG mucosa shows no aneuploid. The positivity of DNA aneuploid tends to increase with the progression of intestinal metaplasia. In addition, telomere length and the DNA index show a reverse correlation. It is speculated that the shorter the telomere length the more amplificative activity the DNA. Telomere length and increased DNA index may be a predictor of stomach carcinogenesis.