Cell cycle, CDKs and cancer: a changing paradigm
gaochen 添加于 2009-10-4 11:59
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作 者
Malumbres M, Barbacid M
摘 要
Tumour-associated cell cycle defects are often mediated by alterations in cyclin-dependent kinase (CDK) activity. Misregulated CDKs induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, mammalian CDKs are essential for driving each cell cycle phase, so therapeutic strategies that block CDK activity are unlikely to selectively target tumour cells. However, recent genetic evidence has revealed that, whereas CDK1 is required for the cell cycle, interphase CDKs are only essential for proliferation of specialized cells. Emerging evidence suggests that tumour cells may also require specific interphase CDKs for proliferation. Thus, selective CDK inhibition may provide therapeutic benefit against certain human neoplasias. -
详细资料
- 关键词: Animals; *Cell Cycle; Cell Proliferation; Chromosomal Instability; Chromosome Aberrations; Cyclin E/physiology; Cyclin-Dependent Kinases/antagonists & inhibitors/*physiology; Cyclins/physiology; DNA Damage; Humans; Mitosis; Neoplasms/drug therapy/genetics/*pathology; Neoplastic Stem Cells/cytology; Protein Kinase Inhibitors/therapeutic use
- 文献种类:期刊
- 期刊名称: Nature Reviews. Cancer
- 期刊缩写: Nat Rev Cancer
- 期卷页: 2009年 第9卷 第3期 153-166页
- 地址: Cell Division and Cancer Group, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncologicas (CNIO), 28029 Madrid, Spain
- ISBN: 1474-1768
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