南方医科大学学报

南方医科大学学报 ›› 2016, Vol. 36 ›› Issue (06): 751-.

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p16INK4a蛋白可作为乳腺癌特异性分子标志

杨军，黄小钟，郭睿，黄莺，康安静，靳耀锋，陈晓黎，李宗芳   

  • 出版日期:2016-06-20 发布日期:2016-06-20

p16INK4a protein is a specific molecular biomarker of breast cancer

  • Online:2016-06-20 Published:2016-06-20

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摘要： 目的探讨p16INK4a 蛋白在乳腺癌中的表达及其临床意义。方法收集2014 年~2015 年间手术切除的132 例乳腺癌标 本，采用罗氏全自动免疫组化染色仪进行免疫组织化学染色，检测ER、PR、Her-2、Ki67、CK5/6、和p16INK4a表达，并按照不同 表达模式进行结果判读和分子分型，观察p16INK4在乳腺癌中的表达及其与乳腺癌免疫表型、分子亚型及临床指标的相关性。 结果132例浸润性乳腺癌中Luminal A型58例、Luminal B型32例、Her-2型21例、basal-like（BLBC）型12例、Normal-like型9 例。p16INK4a蛋白表达阴性（0）、弱阳性（1+）、阳性（2+）和强阳性（3+）表达样本分别占总数的5.30%（7/132）、11.36%（15/132）、 30.30%（40/132）、53.03%（70/132）。按照p16INK4a表达强度，将阴性（0）和弱阳性（1+）病例合并为阴性组（≤1+）、将阳性（2+） 和强阳性（3+）病例合并为阳性组（≥2+），p16INK4a 阴性（≤1+）表达率为16.67%（22/132）、p16INK4a 阳性（≥2+）表达率为 83.33%（110/132）。按照构成比进行统计分析，发现p16INK4a蛋白的表达强度除在不同年龄分组中具有统计学差异（P<0.05） 之外，与ER、PR、Her-2及分子分型和是否存在转移之间均无统计学差异（P>0.50）。结论p16INK4A代偿性高表达是浸润性乳 腺癌细胞周期异常的主要机制，且p16INK4A可作为浸润性乳腺癌细胞特异性的分子标志，采用IHC技术检测p16 INK4a 的表 达不仅为乳腺癌诊断提供了一种重要方法，也为乳腺癌的机制研究提供有价值的信息。

Abstract: Objective To investigate the expression of p16INK4a protein in breast cancer and analyze its clinical significance. Methods A total of 132 surgical specimens of primary breast cancer obtained between 2014 and 2015 were examined for expressions of ER, PR, CK5/6, Her-2 and p16INK4a proteins using immunohistochemistry. Results The breast cancer samples were classified into 5 molecular subtypes, namely Luminal A (58 cases), Luminal B (32 cases), Her-2-positive (21 cases), basal-like (12 cases) and normal-like (9 cases) types. p16INK4a expression was negative in 7/132 (5.30%) cases, weakly positive in 15/132 (11.36%) cases, positive in 40/132 (30.30%) cases, and strongly positive in 70/132 (53.03%) cases. When categorizing negative and weakly positive cases into negative group and the positive and strongly positive cases into positive group, the total negative and positive expression rates of p16INK4a were 16.67% (22/132) and 83.33% (110/132) in the carcinoma tissues. Statistical analysis showed the expression intensity of p16INK4a differed significantly between the age groups (P<0.05) but was not significantly correlated with ER, PR, Her-2, molecular subtypes or metastasis of the tumors. Conclusion The compensatory high expression of p16INK4a is the main mechanism of cell cycle deregulation in invasive breast cancer and can be an important specific molecular marker for invasive breast cancer.