Esposito V, Baldi A, De Luca A, Tonini G, Vincenzi B, Santini D, Persichetti P, Mancini A, Citro G, Baldi F, Groeger A M, Caputi M
International Society for the Study of Comparative Oncology (ISSCO), Silver Spring, MD 20906, USA.
J Clin Pathol. 2005 Jul;58(7):734-9. doi: 10.1136/jcp.2004.023531.
Experimental evidence suggests that lung cancer development and progression can be linked to an increased proliferation rate.
AIMS/METHODS: To evaluate the immunohistochemical expression of seven components of the cell cycle machinery in a series of well characterised non-small cell lung cancer (NSCLC) specimens (n = 105).
Multivariate analysis revealed that simultaneous loss of expression of three of these factors--cyclin D1, the cyclin dependent kinase inhibitor p16, and the tumour suppressor retinoblastoma protein Rb2/p130--correlated with survival, confirming the hypothesis that the cyclin D1-p16-retinoblastoma tumour suppressor pathway is inactivated in most lung cancer samples.
These results suggest that loss of control of cell cycle checkpoints is a common occurrence in lung cancer and support the idea that functional cooperation between different cell cycle regulatory proteins constitutes another level of regulation in cell growth control and tumour suppression.
实验证据表明肺癌的发生和发展可能与增殖率增加有关。
目的/方法：评估一系列特征明确的非小细胞肺癌（NSCLC）标本（n = 105）中细胞周期机制的七个组成部分的免疫组化表达。
多变量分析显示，细胞周期蛋白D1、细胞周期蛋白依赖性激酶抑制剂p16和肿瘤抑制蛋白视网膜母细胞瘤蛋白Rb2/p130这三种因子的表达同时缺失与生存率相关，证实了在大多数肺癌样本中细胞周期蛋白D1-p16-视网膜母细胞瘤肿瘤抑制途径失活的假设。
这些结果表明细胞周期检查点失控在肺癌中很常见，并支持不同细胞周期调节蛋白之间的功能合作构成细胞生长控制和肿瘤抑制的另一层次调节的观点。
