期刊
CANCER CELL
卷 9, 期 1, 页码 23-32出版社
CELL PRESS
DOI: 10.1016/j.ccr.2005.12.012
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资金
- NATIONAL CANCER INSTITUTE [R01CA083688] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA083688] Funding Source: Medline
Cyclin D1 is overexpressed in the majority of human breast cancers. We previously found that mice lacking cyclin D1 are resistant to mammary carcinomas triggered by the ErbB-2 oncogene. In this study, we investigated which function of cyclin D1 is required for ErbB-2-driven mammary oncogenesis. We report that the ability of cyclin D1 to activate cyclin-dependent kinase CDK4 underlies the critical role for cyclin D1 in breast cancer formation. We also found that the continued presence of CDK4-associated kinase activity is required to maintain breast tumorigenesis. We analyzed primary human breast cancers and found high cyclin D1 levels in a subset (similar to 25%) of Erb B-2-overexpressing tumors. We propose that this subset of breast cancer patients might benefit from inhibiting CDK4 kinase.
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