论文部分内容阅读
目的：细胞周期中G1／S转换受到G1期的细胞周期蛋白及细胞周期蛋白的依赖激酶（CDKs）和它们的抑制剂的调节，cyclinD1／CDK4复合物磷酸化（pRB）基因产物、P16与cyclinD1竞争性地抑制CDK4，这些蛋白质的不正常表达就使细胞增殖失控，进而导致肿瘤的形成和发展。本研究从细胞周期调控的角度来探讨喉鳞状细胞癌的发生、发展与CDK4、cyclinD1及P16的关系。方法：用SP免疫组织化学的方法，检测了105例喉癌（其中声门上癌51例，声门癌54例）及28例声带息肉中CDK4、cyclinD1、P16蛋白表达的水平。结果显示：在喉癌组织中cyclinD1的表达以＋＋～＋＋＋为主，而在声带息肉组织中以阴性及弱阳性为主。它们之间存在着显著性的差异（P＜0．05）；而同样P16的表达在喉癌及对照组之间的差异非常显著（P＜0．001）。P16、CDK4的表达在声门上癌与声门癌之间差异显著，P值分别为P=0．002，P=0．021。经Spearman相关分析得出：喉癌组织中CDK4的表达与P16的表达和cyclinD1的表达具有相关性，相关系数分别为0．235、0．253。伴转移的喉癌组织中CDK4的表达与cyclinD1的表达相关明显，相关系数r=0．534。而在非转移的喉癌组织中CDK4与P16相关，相关系数r=0．253。由此我们推论：在喉癌的发生、发展中CDK4、cyclinD1及P16是共
PURPOSE: The G1 / S transition in the cell cycle is regulated by cyclin G1 and cyclin dependent kinases (CDKs) and their inhibitors, cyclinD1 / CDK4 complex phosphorylation (pRB) gene product, P16 and cyclinD1 CDK4 is competitively repressed, and the abnormal expression of these proteins leads to uncontrolled cell proliferation, leading to tumor formation and development. This study from the perspective of cell cycle regulation to explore the occurrence and development of laryngeal squamous cell carcinoma and CDK4, cyclinD1 and P16. Methods: The expressions of CDK4, cyclinD1 and P16 in 105 cases of laryngeal carcinoma (51 cases of supraglottic carcinoma and 54 cases of glottic carcinoma) and 28 cases of vocal cord polyps were detected by SP immunohistochemistry. The results showed that the expression of cyclinD1 was mainly +++ +++ in laryngeal squamous cell carcinoma, but negative and weakly positive in vocal cord polyps. There was a significant difference between them (P <0.05), while the same P16 expression in laryngeal cancer and the control group differences were significant (P <0.001). P16, CDK4 expression in the supraglottic cancer and glottic cancer significant difference between the P values were P = 0.002, P = 0.021. Spearman correlation analysis showed that: the expression of CDK4 in laryngeal carcinoma tissue was correlated with the expression of P16 and the expression of cyclinD1, the correlation coefficients were 0.235,0.253. The expression of CDK4 correlated with the expression of cyclinD1 in laryngeal carcinoma with metastasis, the correlation coefficient was r = 0.534. However, CDK4 was associated with P16 in non-metastatic laryngeal carcinoma with a correlation coefficient of r = 0.253. Thus we deduce: in the occurrence of laryngeal cancer, CDK4, cyclinD1 and P16 are a total of