胰腺癌组织中CD59、Ki67、P16的表达与相关性分析

发布时间：2018-11-24 14:07

【摘要】：目的观察补体调节蛋白CD59、肿瘤增殖抗原Ki67和抑癌基因P16在胰腺癌组织中的表达情况,分析三者与胰腺癌TNM分期、病理分化等的相关性,为胰腺癌发生的分子机制、诊断与治疗提供实验依据。方法选取40例胰腺癌组织标本,另选35例手术切除的胰腺癌旁组织,应用免疫组化(S-P)法,检测胰腺癌组和胰腺癌旁组中CD59、Ki67与P16基因的表达,以PBS液代替一抗作为阴性对照,选已知阳性切片作为阳性结果对照,将胰腺癌组织与胰腺癌旁组织染色,统一评分标准进行结果比较,观察两组中CD59、Ki67与P16的表达情况,所有数据经统计学软件SPSS22.0处理后进行统计。结果在40例胰腺癌组织标本中,CD59阳性表达率65%;Ki67的阳性表达率77.5%;P16阳性表达率42.5%。癌旁对照组中,CD59阳性表达率34.29%;Ki67阳性表达率51.43%;P16阳性表达率88.57%。胰腺癌组中CD59、Ki67的阳性表达率较正常对照组明显升高;相反,胰腺癌组中P16阳性表达率低于癌旁对照组。CD59、Ki67、P16在胰腺癌组与癌旁对照组的表达差异均有显著统计学意义,P0.05。胰腺癌的肿瘤分化程度和临床分期、附近淋巴结转移、远处转移各组间与CD59和Ki67表达强度的比较,差异均有统计学意义,P0.05。即低分化型胰腺癌组中CD59、Ki67的表达强度高于高、中分化组;Ⅲ+Ⅳ期组CD59、Ki67表达强度高于Ⅰ+Ⅱ期组;发生附近淋巴结与远处转移组中CD59、Ki67的表达高于未转移组。胰腺癌的分化程度和临床分期、附近淋巴结转移各组间与P16表达强度的比较均有统计学意义,P0.05,发生远处转移组中P16表达无明显意义P=0.05。高、中分化型胰腺癌组中P16的表达强度高于低分化组;Ⅲ+Ⅳ期组中P16表达强度高于Ⅰ+Ⅱ期组;发生附近淋巴结组中Ki67表达高于未转移组。胰腺癌的分化程度、临床分期、附近淋巴结转移、远处转移与CD59表达均呈正相关,P0.05,r值分别为:0.643,0.564,0.598,0.443;而年龄、性别与CD59表达强度间均无明显相关,P0.05;胰腺癌的分化程度、临床分期、附近淋巴转移、远处转移与Ki67表达均呈正相关,P0.05,r值分别为:0.670,0.652,0.734,0.518;年龄、性别与Ki67无相关性,P0.05;胰腺癌的分化程度、临床分期、附近淋巴转移、远处转移与P16表达均呈负相关,P0.05,r值分别为:-0.673,-0.387,-0.551,-0.315,年龄、性别与P16表达无相关性,P0.05。胰腺癌组中CD59与Ki67存在正相关,P0.05,r=0.734;CD59与P16存在负相关,P0.05,r=-0.580;Ki67与P16存在负相关,P0.05,r值-0.553。结论CD59、Ki67高表达与胰腺癌的分化程度、临床分期、淋巴结转移有关,可能成为胰腺癌早期诊断的参考指标之一。P16在胰腺癌组织中表达降低,且与胰腺癌分化程度、临床分期呈负相关,尤其晚期患者更为显著,故P16可以作为诊断胰腺癌晚期的提示信号。CD59在胰腺癌组织中表达升高,而且CD59有可能成为胰腺癌预后及靶向治疗的重要分子靶标。
[Abstract]:Objective to investigate the expression of complement regulated protein CD59, (CD59,) tumor proliferating antigen (Ki67) and tumor suppressor gene P16 (P16) in pancreatic carcinoma, and to analyze the relationship between them and TNM stage and pathological differentiation of pancreatic carcinoma, which may be the molecular mechanism of pancreatic carcinoma. Diagnosis and treatment provide experimental basis. Methods the expression of CD59,Ki67 and P16 genes in pancreatic carcinoma and paracancreatic tissues were detected by immunohistochemistry (S-P) in 40 cases of pancreatic carcinoma and 35 cases of paracancreatic tissues. Using PBS solution instead of first antibody as negative control and known positive sections as positive result control, the tissues of pancreatic cancer and adjacent tissues of pancreatic cancer were stained, and the results were compared according to the unified scoring criteria. The expression of CD59,Ki67 and P16 in the two groups was observed. All the data were processed by statistical software SPSS22.0. Results in 40 cases of pancreatic carcinoma, the positive expression rate of CD59 was 65.The positive rate of P16 was 77.5% and the positive rate of P16 was 42.5%. In the paracancerous control group, the positive expression rate of CD59 was 34.29% and the positive rate of P16 was 51.43% and 88.57%. The positive expression rate of CD59,Ki67 in pancreatic cancer group was significantly higher than that in normal control group. On the contrary, the positive expression rate of P16 in pancreatic cancer group was lower than that in paracancerous control group. There was significant difference in expression of CD59,Ki67,P16 between pancreatic cancer group and paracancerous control group (P0.05). There were significant differences in tumor differentiation and clinical stage, lymph node metastasis and distant metastasis with CD59 and Ki67 expression in all groups (P 0.05). The expression of CD59,Ki67 in poorly differentiated pancreatic carcinoma group was higher than that in moderately differentiated group, the expression of CD59,Ki67 in stage 鈪，

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