期刊
SCIENCE
卷 375, 期 6577, 页码 158-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.abc1495
关键词
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资金
- Claudia Adams Barr Program for Innovative Basic Cancer Research Award
- NIH [R50CA243769, R01CA202634, CA236226, P50CA168504, P01CA250959]
Cyclin-dependent kinases 4 and 6, along with their activation partners, D-type cyclins, play a crucial role in connecting the extracellular environment with the cell cycle machinery. Inhibiting CDK4/6 has shown success in treating hormone receptor-positive breast cancers and may have potential applications in other tumor types. Recent research has shown that CDK4/6 inhibition affects various cellular functions, including tumor cell metabolism and anti-tumor immunity.
Cyclin-dependent kinases 4 and 6 (CDK4 and CDK6) and their activating partners, D-type cyclins, link the extracellular environment with the core cell cycle machinery. Constitutive activation of cyclin D-CDK4/6 represents the driving force of tumorigenesis in several cancer types. Small-molecule inhibitors of CDK4/6 have been used with great success in the treatment of hormone receptor-positive breast cancers and are in clinical trials for many other tumor types. Unexpectedly, recent work indicates that inhibition of CDK4/6 affects a wide range of cellular functions such as tumor cell metabolism and antitumor immunity. We discuss how recent advances in understanding CDK4/6 biology are opening new avenues for the future use of cyclin D-CDK4/6 inhibitors in cancer treatment.
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