Journal
CANCER CELL
Volume 34, Issue 1, Pages 9-20Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2018.03.023
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Funding
- NIH/NCI Cancer Center [P30 CA008748]
- NCI Soft Tissue Sarcoma SPORE [CA140146]
- Maloris Foundation
- Linn Fund from Cycle for Survival
- Heidi Connery Memorial Research Grant from the Sarcoma Foundation of America
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CDK4/6 inhibitors are among a new generation of therapeutics. Building upon the striking success of the combination of CDK4/6 inhibitors and the hormone receptor antagonist letrozole in breast cancer, many other combinations have recently entered clinical trials in multiple diseases. To achieve maximal benefit with CDK4/6 inhibitors it will be critical to understand the cellular mechanisms by which they act. Here we highlight the mechanisms by which CDK4/6 inhibitors can exert their anti-tumor activities beyond simply enforcing cytostatic growth arrest, and discuss how this knowledge may inform new combinations, improve outcomes, and modify dosing schedules in the future.
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