Requirement for CDK4 kinase function in breast cancer

Qunyan Yu, Ewa Sicinska, Yan Geng, Marie Ahnström, Agnieszka Zagozdzon, Yinxin Kong, Humphrey Gardner, Hiroaki Kiyokawa, Lyndsay N. Harris, Olle Stål, Piotr Sicinski*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

268 Scopus citations

Abstract

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 (∼25%) of ErbB-2-overexpressing tumors. We propose that this subset of breast cancer patients might benefit from inhibiting CDK4 kinase.

Original languageEnglish (US)
Pages (from-to)23-32
Number of pages10
JournalCancer Cell
Volume9
Issue number1
DOIs
StatePublished - Jan 2006

ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research

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