肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2013年
5期
316-319
,共4页
崔阳阳%陆建波%王京晔%沈剑%习杨彦彬%王春艳
崔暘暘%陸建波%王京曄%瀋劍%習楊彥彬%王春豔
최양양%륙건파%왕경엽%침검%습양언빈%왕춘염
结肠肿瘤%Ki-67%Livin%Survivin
結腸腫瘤%Ki-67%Livin%Survivin
결장종류%Ki-67%Livin%Survivin
Colon neoplasms%Ki-67%Livin%Survivin
目的 分析Ki-67、Survivin和Livin蛋白在结肠腺上皮中的表达,探讨其在结肠腺癌发生、发展过程中增殖能力的变化和抗凋亡因素的影响.方法 取结肠腺上皮轻度非典型增生36例,中度非典型增生34例,重度非典型增生18例,高分化腺癌35例,中分化腺癌27例,低分化腺癌35例,癌旁组织34例.采用免疫组织化学方法结合组织芯片技术分别检测Ki-67、Survivin和Livin蛋白在不同组间的表达.结果 结肠上皮轻度非典型增生、中度非典型增生、重度非典型增生、高分化腺癌、中分化腺癌、低分化腺癌和癌旁组织Ki-67的阳性表达率为(21.56±19.20)％、(37.44±17.41)％、(36.17±17.41)％、(55.29±16.13)％、(44.89±29.67)％、(45.11 ±29.24)％及(43.94±28.84)％,Ki-67在各组间表达差异有统计学意义(F=6.796,P＜0.05).Survivin和Livin阳性表达率分别为:13.8％、44.1％、77.8％、85.7％、85.1 ％、91.4 ％、91.1％和2.7％、38.2％、55.6％、100.0％、77.8％、80.0％、79.4％.Survivin和Livin在各组间表达差异有统计学意义(X2值分别为84.754、95.200,P＜0.05).Livin与Ki-67表达有相关性(r=0.360,P＜0.05),而Survivin与Ki-67表达无相关性(r=0.044,P＞0.05).结论 结肠腺上皮从轻度非典型增生到高分化腺癌细胞增殖形成一个高峰,又逐渐下降到低分化腺癌形成一个平台.结肠上皮发生癌变时,细胞的增殖能力显著增强,凋亡抑制也达高峰,肿瘤细胞发生了恶性生物学行为的转变；结肠癌周微环境使得癌旁组织增殖能力增强,进一步促进肿瘤的发生、发展；Livin能够抑制凋亡,而且与Survivin协同作用,在结肠腺癌发生、发展中发挥一定的作用.
目的 分析Ki-67、Survivin和Livin蛋白在結腸腺上皮中的錶達,探討其在結腸腺癌髮生、髮展過程中增殖能力的變化和抗凋亡因素的影響.方法 取結腸腺上皮輕度非典型增生36例,中度非典型增生34例,重度非典型增生18例,高分化腺癌35例,中分化腺癌27例,低分化腺癌35例,癌徬組織34例.採用免疫組織化學方法結閤組織芯片技術分彆檢測Ki-67、Survivin和Livin蛋白在不同組間的錶達.結果 結腸上皮輕度非典型增生、中度非典型增生、重度非典型增生、高分化腺癌、中分化腺癌、低分化腺癌和癌徬組織Ki-67的暘性錶達率為(21.56±19.20)％、(37.44±17.41)％、(36.17±17.41)％、(55.29±16.13)％、(44.89±29.67)％、(45.11 ±29.24)％及(43.94±28.84)％,Ki-67在各組間錶達差異有統計學意義(F=6.796,P＜0.05).Survivin和Livin暘性錶達率分彆為:13.8％、44.1％、77.8％、85.7％、85.1 ％、91.4 ％、91.1％和2.7％、38.2％、55.6％、100.0％、77.8％、80.0％、79.4％.Survivin和Livin在各組間錶達差異有統計學意義(X2值分彆為84.754、95.200,P＜0.05).Livin與Ki-67錶達有相關性(r=0.360,P＜0.05),而Survivin與Ki-67錶達無相關性(r=0.044,P＞0.05).結論 結腸腺上皮從輕度非典型增生到高分化腺癌細胞增殖形成一箇高峰,又逐漸下降到低分化腺癌形成一箇平檯.結腸上皮髮生癌變時,細胞的增殖能力顯著增彊,凋亡抑製也達高峰,腫瘤細胞髮生瞭噁性生物學行為的轉變；結腸癌週微環境使得癌徬組織增殖能力增彊,進一步促進腫瘤的髮生、髮展；Livin能夠抑製凋亡,而且與Survivin協同作用,在結腸腺癌髮生、髮展中髮揮一定的作用.
목적 분석Ki-67、Survivin화Livin단백재결장선상피중적표체,탐토기재결장선암발생、발전과정중증식능력적변화화항조망인소적영향.방법 취결장선상피경도비전형증생36례,중도비전형증생34례,중도비전형증생18례,고분화선암35례,중분화선암27례,저분화선암35례,암방조직34례.채용면역조직화학방법결합조직심편기술분별검측Ki-67、Survivin화Livin단백재불동조간적표체.결과 결장상피경도비전형증생、중도비전형증생、중도비전형증생、고분화선암、중분화선암、저분화선암화암방조직Ki-67적양성표체솔위(21.56±19.20)％、(37.44±17.41)％、(36.17±17.41)％、(55.29±16.13)％、(44.89±29.67)％、(45.11 ±29.24)％급(43.94±28.84)％,Ki-67재각조간표체차이유통계학의의(F=6.796,P＜0.05).Survivin화Livin양성표체솔분별위:13.8％、44.1％、77.8％、85.7％、85.1 ％、91.4 ％、91.1％화2.7％、38.2％、55.6％、100.0％、77.8％、80.0％、79.4％.Survivin화Livin재각조간표체차이유통계학의의(X2치분별위84.754、95.200,P＜0.05).Livin여Ki-67표체유상관성(r=0.360,P＜0.05),이Survivin여Ki-67표체무상관성(r=0.044,P＞0.05).결론 결장선상피종경도비전형증생도고분화선암세포증식형성일개고봉,우축점하강도저분화선암형성일개평태.결장상피발생암변시,세포적증식능력현저증강,조망억제야체고봉,종류세포발생료악성생물학행위적전변；결장암주미배경사득암방조직증식능력증강,진일보촉진종류적발생、발전；Livin능구억제조망,이차여Survivin협동작용,재결장선암발생、발전중발휘일정적작용.
Objective To investigate the expression of Ki-67,Survivin,Livin in dysplasia,colon carcinogenesis and para-carcinoma tissues,and to discuss the variation of cell proliferous capability in colon carcinogenesis and antiapoptosis factors.Methods 219 specimens were composed of mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma,para-carcinoma tissues of 36,34,18,35,27,35 and 34 cases.Detected the expression of Ki-67,Survivin and Livin with tissue microarray and immunohistochemical methods.All data were statistically analyzed by SPSS 17.0.Results In mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma and para-carcinoma tissues the expression of Ki-67 were (21.56 ± 19.20)％,(37.44 ± 17.41)％,(36.17 ± 17.41)％,(55.29 ± 16.13)％,(44.89 ± 29.67)％,(45.11 ± 29.24)％,(43.94 ± 28.84)％,Survivin were 13.8 ％,44.1％,77.8 ％,85.7 ％,85.1％,91.4 ％,91.1％,and Livin were 2.7 ％,38.2 ％,55.6 ％,100.0 ％,77.8 ％,80.8 ％,79.4 ％.The differences of Ki-67,Survivin and Livin expression in each group were statistically significant (F =6.796,X2 =81.754,X2 =95.200,all P ＜ 0.05).Ki-67 was significantly correlated with expression of Livin (r =0.360,P ＜ 0.05) and no correlated with expression of Survivin (r =0.044,P ＞ 0.05).Conclusion Colonic epithelium from mild atypical hyperplasia to proliferation of well-differentiated adenocarcinoma cells formed a peak,and gradually down to poorly differentiated adenocarcinoma formed a platform.When the colon epithelial cells to become cancerous,the capability of cell proliferation will significantly enhance,apoptosis inhibition will reach the peak and the tumor cell will happen the changes of malignant biological behavior.Tumor microenvironment may promote the cell proliferation in para-carcinoma tissues and the development of colon cancer.Livin may inhibit apoptosis and promot the progression in synergistic mechanism importing with Survivin,which play a role in the development of colonic adenocarcinoma.
