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Requirement for CDK4 kinase function in breast cancer
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts.
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts.
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts.
Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi. Linköpings universitet, Hälsouniversitetet.
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2006 (engelsk)Inngår i: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 9, nr 1, s. 23-32Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
2006. Vol. 9, nr 1, s. 23-32
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URN: urn:nbn:se:liu:diva-36168DOI: 10.1016/j.ccr.2005.12.012Lokal ID: 30325OAI: oai:DiVA.org:liu-36168DiVA, id: diva2:257016
Tilgjengelig fra: 2009-10-10 Laget: 2009-10-10 Sist oppdatert: 2017-12-13

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