Funk J O, Kind P
Dermatologische Klinik und Poliklinik, Ludwig-Maximilians-Universität, München.
Hautarzt. 1997 Mar;48(3):157-65. doi: 10.1007/s001050050563.
During the past years the elucidation of cell cycle regulation has revolutionized our understanding of cancer development. Many new genes have been identified which promote genetic instability when mutated. They encode cyclins, inhibitors of cyclin-dependent kinases (CDKs) or other cell cycle regulators. The regulation of the CDK activities in different phases of the cell cycle controls the correct process of DNA synthesis and replication. Complex signal transduction systems, so-called checkpoints, regulate growth arrest, DNA repair and programmed cell death (apoptosis) and thereby prevent the formation of tumour cells. An overview is presented on the molecular mechanisms of cell cycle control and their significance for genetic stability. The functions of proto-oncogenes (e.g., c-myc) and tumour-suppressor genes (e.g., p53) in this context is described. In particular, recent advances in the understanding of skin carcinogenesis, the role of UV radiation and cancer therapy are discussed.
在过去几年中,细胞周期调控机制的阐明彻底改变了我们对癌症发展的理解。许多新基因已被鉴定出来,这些基因在发生突变时会促进基因不稳定。它们编码细胞周期蛋白、细胞周期蛋白依赖性激酶(CDK)抑制剂或其他细胞周期调节因子。细胞周期不同阶段中CDK活性的调节控制着DNA合成和复制的正确过程。复杂的信号转导系统,即所谓的检查点,调节生长停滞、DNA修复和程序性细胞死亡(凋亡),从而防止肿瘤细胞的形成。本文概述了细胞周期控制的分子机制及其对遗传稳定性的意义。描述了原癌基因(如c-myc)和肿瘤抑制基因(如p53)在此背景下的功能。特别讨论了皮肤癌发生机制、紫外线辐射的作用以及癌症治疗方面的最新进展。