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目的:探讨细胞周期素D1、P16蛋白在子宫内膜癌中的表达及其临床意义。方法:采用免疫组化法(SP法)检测CyclinD1、P16蛋白在52例子宫内膜癌和26例正常子宫内膜中的表达,并对比两者在子宫内膜癌不同的病理分级、肌层浸润、临床分期中的表达差异。结果:CyclinD1基因在子宫内膜癌组织中阳性表达率为55.8%(29/52),显著高于对照组的11.5%(3/26)(P<0.01)。子宫内膜癌CyclinD1阳性表达患者的肿瘤细胞分化程度低且多有肌层浸润。P16蛋白在内膜癌组阳性表达率为57.7%(30/52),显著低于对照组的88.5%(23/26),其在子宫内膜癌不同组织分化程度、不同临床分期及有无淋巴转移组间表达阳性率比较有统计学差异(P<0.05)。内膜癌组CyclinD1与P16协同异常表达率为30.8%,协同正常表达率为32.7%。经等级相关分析,CyclinD1与P16表达未见相关关系。结论:子宫内膜癌组织中P16蛋白和CyclinD1的表达异常,检测结果有助于分析子宫内膜癌的分化程度、转移侵蚀及预后。两者协同异常表达表明肿瘤发生是多因素、多步骤、多阶段、多种癌基因和抑癌基因参与的复杂病理过程。
Objective: To investigate the expression of cyclin D1, P16 protein in endometrial carcinoma and its clinical significance. Methods: The expressions of CyclinD1 and P16 protein in 52 cases of endometrial carcinoma and 26 cases of normal endometrium were detected by immunohistochemistry (SP method), and compared their different pathological grades in endometrial carcinoma, Infiltration, clinical stage of expression differences. Results: The positive rate of CyclinD1 in endometrial carcinoma was 55.8% (29/52), which was significantly higher than that in control group (11.5%, 3/26) (P <0.01). Endometrial cancer CyclinD1-positive patients with low degree of tumor cell differentiation and more myometrial invasion. The positive rate of P16 protein in endometrial carcinoma was 57.7% (30/52), which was significantly lower than that in control group (88.5%, 23/26). The expression of P16 protein in different tissues of endometrial carcinoma with different clinical stages and with or without The positive rate of lymph node metastasis was statistically significant (P <0.05). In endometrial carcinoma group, the abnormal expression rate of CyclinD1 and P16 was 30.8%, and the normal expression rate was 32.7%. The level of correlation analysis, CyclinD1 and P16 expression no correlation. Conclusion: The expression of P16 protein and CyclinD1 in endometrial carcinoma is abnormal. The detection results are helpful to analyze the differentiation, metastasis and prognosis of endometrial carcinoma. Synergistic aberrant expression of both showed that tumorigenesis is a complex pathological process involving multiple factors, multi-step, multi-stage, multiple oncogenes and tumor suppressor genes.