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作 者:铁朝荣[1] 陈建钢[1] 范崇德[1] 李清[1] 李辉
出 处:《临床口腔医学杂志》1998年第2期70-72,共3页Journal of Clinical Stomatology
基 金:湖北省教委资助
摘 要:本文采用免疫组化、PCR技术,检测30例涎腺肿瘤组织中c-myc、P53、Bcl-2蛋白表达和HPV感染。结果显示:多形性腺瘤中,c-myc和P53阳性率分别为50.0%和25.0%,均低于恶性肿瘤阳性率的75.0%和50.8%,两组存在高度显著性差异(P<0.01);15例多形性腺瘤和3例鳞癌中,HPV6.11均为阴性,HPV16.18阳性反应各1例(1/15和1/3)。提示c-myc表达升高,与上皮细胞增殖速度加快及细胞癌变有关;P53蛋白表达,可为判断细胞分化程度的参考指标;HPV16.18具一定协同致癌作用。Bcl-2能引起细胞过度积聚,故为恶性肿瘤的发病机制之一。c-myc,P53 proteins and infections of HPV in salivary gland tumous were detected by immunohistochemical method and PCR. The results showed that in PA, the positive rates of c-myc and P53 were 50. 0% and 25. 0%. Both of them were lower than those of malignant tumours (75. 0% and 50. 8%). there were high defferances between two groups (P<0. 01 ). In 15 cases of PA and 3 cases of SCC, HPV6. 11 rections were all negative, but in 1 case of PA and 1 case of SCC, HPV16.18 staining were positive. The study indicates c-myc expressions were associated with cell proliferation and mutation, P53 overexpression can be a reference for cell differentiation. HPV16. 18 play a cooperation role in carcinogen. Because Bc1- 2 Could bring about cell accumulation, so it is one of mechanism for malignent tumour.
分 类 号:R739.870.2[医药卫生—肿瘤]
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