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Sökning: WFRF:(Ahnström Marie) > (2006) > Requirement for CDK...

Requirement for CDK4 kinase function in breast cancer

Yu, Qunyan (författare)
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts
Sicinska, Ewa (författare)
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts
Geng, Yan (författare)
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts
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Ahnström, Marie, 1976- (författare)
Linköpings universitet,Onkologi,Hälsouniversitetet
Zagozdzon, Agnieszka (författare)
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts
Kong, Yinxin (författare)
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts
Gardner, Humphrey (författare)
Department of Research Pathology, Biogen Idec, Cambridge, Massachusetts
Kiyokawa, Hiroaki (författare)
Department of Molecular Pharmacology and Biochemical Chemistry, Northwestern University, Chicago, Illinois
Harris, Lyndsay N (författare)
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts and Department of Medical Oncology, Dana-Farber Cancer Institute, and Brigham and Women's Hospital, Boston, Massachusetts
Stål, Olle, 1952- (författare)
Linköpings universitet,Onkologi,Hälsouniversitetet
Sicinski, Piotr (författare)
Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, Massachusetts
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 (creator_code:org_t)
Elsevier BV, 2006
2006
Engelska.
Ingår i: Cancer Cell. - : Elsevier BV. - 1535-6108 .- 1878-3686. ; 9:1, s. 23-32
  • Tidskriftsartikel (refereegranskat)
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  • 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.

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MEDICIN

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