乳腺癌组织DAPK和p53及Bc1-2表达及其相互关系的研究

目的:检测乳腺癌组织中死亡相关蛋白激酶(DAPK)、p53和Bcl-2表达,探讨DAPK、p53和Bcl-2在乳腺癌组织中的作用及其相互关系。方法:用免疫组化SP法检测42例乳腺增生组织和68例乳腺浸润性癌组织中DAPK、p53和Bcl-2的表达水平,分析它们与乳腺癌临床病理的关系。结果:p53蛋白在乳腺增生组织中的表达为阴性,在乳腺癌组织中阳性表达率为51.5%(35/68);p53的阳性率与乳腺癌的组织学分级、淋巴结转移呈正相关。乳腺癌组织中Bcl-2阳性表达率为69.1%(47/68),明显高于乳腺增生组织;Bcl-2的阳性率与乳腺癌的肿瘤大小、淋巴结转移呈负相关。DAPK在乳腺癌组织中的阳性表达率为42.6%(29/68),明显低于乳腺增生组织;DAPK的阳性率与乳腺癌的病理分型、组织学分级、淋巴结转移、p53及Bcl-2呈负相关。结论:DAPK、p53和Bcl-2蛋白可作为预测乳腺癌生物学行为的参考指标。DAPK可能抑制乳腺癌的侵袭转移,这个作用可能与p53、Bcl-2相关。

Expressions of DAPK, p53 and Bcl-2 proteins in breast carcinoma tissues and their correlation

OBJECTIVE:To investigate the expressions of p53,Bcl-2 and DAPK in breast carcinoma and breast hyperplasia tissues and explore their clinical significance.METHODS:The expressions of DAPK,p53 and Bcl-2 were tested in 42 cases of breast hyperplasia and 68 cases of invasive breast carcinoma by SP immunohistochemical methods.The significance of these markers was evaluated by analyzing the correlation between these markers and the pathologically biological features of breast cancer.RESULTS:p53 expression was negative in breast hyperplasia tissue while was positive in 51.5%(35/68)of cancer tissue.There was a significant positive correlation between the expression of p53 and the histological grade,pathological subtype,lymph-node metastasis.The expression of Bcl-2 in breast tissues was 69.1%(47/68)which was significantly higher than that in hyperplasia tissue and a positive correlation was found between the expression of Bcl-2 and tumor diameter and lymph node metastasis.The expression of DAPK in breast carcinoma tissues was 42.6%(29/68)which was significantly lower than that in the hyperplasia tissues and a negative correlation was found between its expression and the histological grade,pathological subtype,lymph-node metastasis,p53 and Bcl-2.CONCLUSIONS:The expressions of DAPK,p53 and Bcl-2 can be used as important biological markers for breast cancer.DAPK may play an important role in the development of breast cancer.Down-regulation of the expressions of Bcl-2 and mutation p53 is probably one of its molecular mechanisms.