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作 者:王晓薇[1] 郭小光[2] 鲍力[3] 王燕[1] 曹虹然[4] 白雪峰[1]
机构地区:[1]首都医科大学附属北京妇产医院乳腺科,北京市100006 [2]内蒙古自治区包头市第七医院外科 [3]内蒙古自治区包头市第七医院内科 [4]内蒙古自治区包头市第七医院病理科
出 处:《中国肿瘤临床》2005年第10期564-567,共4页Chinese Journal of Clinical Oncology
基 金:包头市科学技术局科研基金资助(编号:BK2003004)
摘 要:目的:检测Bcl-2、Bad基因蛋白在乳腺良、恶性病变组织中的表达,探讨细胞凋亡调控基因在乳腺癌发生发展中的作用。方法:应用免疫组织化学染色SABC法,观察19例乳腺单纯性增生,20例乳腺非典型增生,48例乳腺癌组织中Bcl-2、Bad蛋白的表达,另取8例正常乳腺组织作对照。结果:Bcl-2在正常组和乳腺单纯性增生组100%表达,乳腺非典型增生组表达率为85.0%,乳腺癌组为58.3%,两组比较有显著差异(χ2=4.48,P<0.05)。Bad蛋白在正常对照组为87.5%表达,乳腺单纯性增生表达率为84.2%,乳腺非典型增生组55.0%,乳腺癌组为47.9%,各组中的表达率与Bcl-2比较有下降趋势。Bcl-2、Bad在各组中表达阳性率有显著性差异(χ2=23.05P<0.001,χ2=11.29P<0.01)。结论:Bcl-2、Bad基因在乳腺癌的恶性转化中可能发生一定作用,可能与乳腺癌细胞凋亡调节有关。Objective: To test the expression of apoptosis regulation gene Bcl-2 and Bad in the benign and malignant breast lesion, and to explore the role of they in the growth and development of breast cancer. Methods: By immunohistochemical methed, the expression of Bcl-2 and Bad gene were observed in eight cases with normal breast tissue, 19 breast hyperplasia and 20 breast atypical, as well as 48 with breast cancer in situs. Eight cases of normal breast tissue were used as the controls. Results: The Bcl-2 gene was 100% positive expression in the 8 cases of normal breast tissues and 19 with breast hypreplasia, and was 85.0% in breast atypical, and was 58.3% in breast cancer. A statistical signification was found between the positive rate of atypical cancer and of breast cancer (χ2=4.48 P<0.05 ). The positive rate of Bad oncoprotein was of lower tendency compared to Bcl-2 of all groups: 87.5% in normal, 84.2% in hyperplasia, 55.0% in atypical, 47.9% in breast cancer, respestively. There was a significant difference between positive rate of Bcl-2 and of bad in each group. (χ2=23.05 P<0.001, χ2=11.29 P<0.01). In the breast cancer group the positive rate of Bcl-2 and Bad oncoprotein was decreasd with a descent in differentiation of tumor. Conclusion: Bcl-2 and Bad oncoprotein may play a role in growth and development of cancer and may relate to the apoptosis regulation of breast cancer.
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