论文部分内容阅读
目的探讨转化生长因子β_1(transforming growth factor β_1,TGF-β_1)及其Ⅰ型受体 TGFβR—I与子宫内膜癌(endometrial carcinoma,EC)发生及转移的关系。方法采用免疫组织化学技术检测子宫内膜癌30例、子宫内膜复杂增生(complex hyperplasia,CH)15例,其中伴有不典型增生9例、正常子宫内膜组织12例中 TGF-β_1及其受体 TGFβR-I 的表达。利用 CD34相关抗原标记血管内皮细胞,计数微血管密度(microvessel density,MVD)。子宫肌层侵蚀面积被选择地染色。结果子宫内膜癌及复杂增生组织中 TGF-β_1表达明显高于正常子宫内膜组织(P<0.01,P<0.05),而前两者之间差异无统计学意义(P>0.05)。TGF-β_1表达水平与子宫内膜癌肌层浸润深度呈正相关(P<0.05)。从正常子宫内膜、复杂增生到子宫内膜癌组织中 TGF-β_1表达逐渐下降甚至缺如,且两两间差异均有统计学意义(P<0.05)。TGFβR-I 表达与肌层浸润深度呈负相关(P<0.05)。子宫内膜癌组织中MVD 高于复杂增生组及正常子宫内膜(P<0.01),与组织学分级、肌层浸润深度及临床分期差异无统计学意义(P>0.05),而与 TGF-β_1差异有统计学意义(P<0.05)。结论 TGF-β_1过度表达可能是子宫内膜癌发生的早期现象,而其促进癌组织的肌层浸润和血管发生,则可能是子宫内膜癌发生转移的机制。TGF-β_1促进子宫内膜癌发生与转移的作用均与 TGFβR-I 表达下降或缺如有关。
Objective To investigate the relationship between the expression of transforming growth factor β_1 (TGF-β_1) and its type Ⅰ receptor TGFβR-I and the occurrence and metastasis of endometrial carcinoma (EC). Methods Thirty cases of endometrial carcinoma and 15 cases of endometrial hyperplasia (CH) were detected by immunohistochemical technique, including 9 cases of atypical hyperplasia and 12 cases of normal endometrium, Receptor TGFβR-I expression. Vascular endothelial cells were labeled with CD34-associated antigen and microvessel density (MVD) was counted. Myometrial erosion area is selectively stained. Results The expression of TGF-β 1 in endometrial carcinoma and complex hyperplasia tissues was significantly higher than that in normal endometrial tissues (P <0.01, P <0.05). There was no significant difference between the two groups (P> 0.05). The expression of TGF-β_1 was positively correlated with the depth of myometrial invasion in endometrial carcinoma (P <0.05). The expression of TGF-β 1 in normal endometrium, complex hyperplasia and endometrial carcinoma gradually decreased or even absent, and the difference between the two groups was statistically significant (P <0.05). TGFβR-I expression was negatively correlated with the depth of myometrial invasion (P <0.05). The MVD in endometrial carcinoma was higher than that in complex hyperplasia and normal endometrium (P <0.01), but not significantly different from histological grade, depth of myometrial invasion and clinical stage (P> 0.05) β_1 difference was statistically significant (P <0.05). Conclusion Overexpression of TGF-β 1 may be an early phenomenon of endometrial cancer, and its promotion of myometrial invasion and angiogenesis may be the mechanism of endometrial cancer metastasis. The role of TGF-β 1 in promoting the occurrence and metastasis of endometrial carcinoma is related to the decrease or absence of TGFβR-I expression.