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

doi:10.1016/j.ccr.2005.12.012

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

Pharmacology

Research output: Contribution to journal › Article › peer-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 language	English (US)
Pages (from-to)	23-32
Number of pages	10
Journal	Cancer Cell
Volume	9
Issue number	1
DOIs	https://doi.org/10.1016/j.ccr.2005.12.012
State	Published - Jan 2006

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

Access to Document

10.1016/j.ccr.2005.12.012

Fingerprint Dive into the research topics of 'Requirement for CDK4 kinase function in breast cancer'. Together they form a unique fingerprint.

Cite this

@article{e3800ebb66024ec39cf6ff73c7e39cfb,

title = "Requirement for CDK4 kinase function in breast cancer",

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.",

author = "Qunyan Yu and Ewa Sicinska and Yan Geng and Marie Ahnstr{\"o}m and Agnieszka Zagozdzon and Yinxin Kong and Humphrey Gardner and Hiroaki Kiyokawa and Harris, {Lyndsay N.} and Olle St{\aa}l and Piotr Sicinski",

note = "Funding Information: The authors thank P. Hinds, M. Landis, W. Hahn, R. Possemato, R. Bronson, L. Zhang, C. Kuperwasser, and members of the Sicinski lab for help, advice, and reagents. This work was supported by an NCI R01 grant CA083688, and by a Susan G. Komen Breast Cancer Foundation grant (BCTR02-2109) to P.S. ",

year = "2006",

month = jan,

doi = "10.1016/j.ccr.2005.12.012",

language = "English (US)",

volume = "9",

pages = "23--32",

journal = "Cancer Cell",

issn = "1535-6108",

publisher = "Cell Press",

number = "1",

}

TY - JOUR

T1 - Requirement for CDK4 kinase function in breast cancer

AU - Yu, Qunyan

AU - Sicinska, Ewa

AU - Geng, Yan

AU - Ahnström, Marie

AU - Zagozdzon, Agnieszka

AU - Kong, Yinxin

AU - Gardner, Humphrey

AU - Kiyokawa, Hiroaki

AU - Harris, Lyndsay N.

AU - Stål, Olle

AU - Sicinski, Piotr

N1 - Funding Information: The authors thank P. Hinds, M. Landis, W. Hahn, R. Possemato, R. Bronson, L. Zhang, C. Kuperwasser, and members of the Sicinski lab for help, advice, and reagents. This work was supported by an NCI R01 grant CA083688, and by a Susan G. Komen Breast Cancer Foundation grant (BCTR02-2109) to P.S.

PY - 2006/1

Y1 - 2006/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=30344470210&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=30344470210&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2005.12.012

DO - 10.1016/j.ccr.2005.12.012

M3 - Article

C2 - 16413469

AN - SCOPUS:30344470210

VL - 9

SP - 23

EP - 32

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 1

ER -