Cell cycle control, genetic instability and cancer

被引:8
作者
Funk, JO
Kind, P
机构
[1] UNIV MUNICH, DERMATOL KLIN & POLIKLIN, D-8000 MUNICH, GERMANY
[2] GSF FORSCHUNGSZENTRUM UMWELT & GESUNDHEIT, INST KLIN MOL BIOL & TUMORGENET, MUNICH, GERMANY
来源
HAUTARZT | 1997年 / 48卷 / 03期
关键词
cell cycle; checkpoint; cyclins; tumour-suppressor genes; apoptosis;
D O I
10.1007/s001050050563
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
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 protooncogenes (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.
引用
收藏
页码:157 / 165
页数:9
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