论文部分内容阅读
细胞循环周期是细胞生长增殖的基础,其内源性调控途径为cyclin-CDK-CKI。eyclin D1与p15都是作用于G_1/S交界处,cyclin D1是细胞周期启动因子,与细胞周期呈正相关;p15是一个CKI分子,作为抑癌基因与细胞增殖呈负相关,其失活主要是甲基化。两者的失衡则导致细胞周期异常、肿瘤的发生。检测其变化,有助于血液病的诊断、治疗及判断预后。通过对其失活机制的研究,应用甲基化抑制剂等抑制其异常,对血液病的治疗将是一个新的发展方向。
Cell cycle is the basis of cell growth and proliferation, and its endogenous regulatory pathway is cyclin-CDK-CKI. Cyclin D1 is a cell cycle initiation factor and has a positive correlation with cell cycle. p15 is a CKI molecule which is negatively correlated as a tumor suppressor gene and cell proliferation, and its inactivation is mainly due to the fact that both eyclin D1 and p15 act on G_1 / S junction Methylation. The imbalance between the two leads to cell cycle abnormalities and tumorigenesis. Detection of changes in blood diseases contribute to the diagnosis, treatment and prognosis. Through the study of its inactivation mechanism, the application of methylation inhibitors to inhibit its abnormalities, the treatment of blood diseases will be a new direction of development.