凋亡的死亡信号受体途径在胆囊癌发生发展中的作用
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The action of death signal receptor pathway of apoptosis in the developmen of gallbladder carcinoma
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    目的:研究凋亡的死亡信号受体途径在胆囊癌发生和发展中的作用。方法:应用SP免疫组化法研究胆囊癌组织中死亡信号受体途径的激活分子FasL蛋白的表达水平及其特征;并运用TUNEL法原位检测肿瘤周围浸润的淋巴细胞的凋亡数量。结果:胆囊癌、胆囊腺瘤、胆囊上皮不典型增生和慢性胆囊炎组织中FasL蛋白的阳性率分别为84.6%(22/26),83.3%(15/18),100%(3/3)和55%(11/20)。FasL蛋白表达在胆囊癌明显高于慢性胆囊炎(P<0.05)。浸润淋巴细胞发生凋亡的数量,在FasL蛋白阳性[FasL(+)]的胆囊癌组织中极显著高于FasL蛋白阴性[FasL(-)]的胆囊癌组织(P<0.01);在FasL(+)的低分化胆囊癌组织中高于FasL(-)的低分化胆囊癌组织(P<0.05);在FasL(+)的NevinI,II,III期胆囊癌组织中高于FasL(-)的NevinI,II,III期胆囊癌组织(P<0.01)。结论:凋亡的死亡信号受体途径参与了胆囊癌的发生发展过程。

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    Abstract:Objective:To study the action of death signal receptor pathway of apoptosis in the development of gallbladder carcinoma. Methods:Streptavidin-biotin-peroxidase immunohistochemistry technique was used to study the expression of Fas L in gallbladder carcinoma tissues,and TUNEL method for in situ detection of the number of apoptotic infiltrating lymphocytes around the tumor. Results:The positive rates of Fas L in gallbladder carcinoma, gallbladder adenoma, dysplasia of gallbladder epithelium and chronic cholecystis were 84.6%(22/26), 83.3%(15/18) ,100%(3/3) and 55%(11/20), respectively. The positive rate of Fas L in gallbladder carcinoma was significantly higher than in chronic cholecystis (P<0.05). The number of apoptotic infiltrating lymphocytes in gallbladder carcinoma of Fas L(+) was significantly higher than in gallbladder carcinoma of Fas L(-)(P<0.01). The number of apoptotic infiltrating lymphocytes in poorly-differentiated gallbladder carcinoma of Fas L(+) was significantly higher than in poorly-differentiated gallbladder carcinoma of Fas L(-)( P<0.05). The number of apoptotic infiltrating lymphocytes in NevinI、II、III gallbladder carcinoma of Fas L(+) was significantly higher than in NevinI,II,III gallbladder carcinoma of Fas L(-)(P<0.01). Conclusions:The death signal receptor pathway of apoptosis plays a role in the development of gallbladder carcinoma.

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徐立宁,邹声泉.凋亡的死亡信号受体途径在胆囊癌发生发展中的作用[J].中国普通外科杂志,2005,14(1):10-.
DOI:10.7659/j. issn.1005-6947.2005.01.010

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  • 在线发布日期: 2005-01-25