期刊
TRENDS IN CELL BIOLOGY
卷 28, 期 11, 页码 911-925出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2018.07.002
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资金
- National Institutes of Health (NIH)/National Cancer Institute (NCI) [P50 CA168504]
- NIH/NCI [CA165962, CA187918, CA210057]
- Department of Defense (DoD) CDMRP BCRP Era of Hope Award [W81XWH-14-1-0191]
- DoD [BC171657]
- Breast Cancer Research Foundation
- Susan G. Komen [CCR18547966]
- Breast Cancer Alliance
- Landry Cancer Biology Research Fellowship
- NATIONAL CANCER INSTITUTE [R01CA187918, R35CA210057, P50CA168504] Funding Source: NIH RePORTER
Pharmacologic inhibitors of cyclin-dependent kinases 4 and 6 (CDK4/6) have recently entered the therapeutic armamentarium of clinical oncologists, and show promising activity in patients with breast and other cancers. Although their chief mechanism of action is inhibition of retinoblastoma (RB) protein phosphorylation and thus the induction of cell cycle arrest, CDK4/6 inhibitors alter cancer cell biology in other ways that can also be leveraged for therapeutic benefit. These include modulation of mitogenic kinase signaling, induction of a senescence-like phenotype, and enhancement of cancer cell immunogenicity. We describe here the less-appreciated effects of CDK4/6 inhibitors on cancer cells, and suggest ways by which they might be exploited to enhance the benefits of these agents for cancer patients.
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