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Cell cycle control in breast cancer cells
Author(s) -
Caldon C. Elizabeth,
Daly Roger J.,
Sutherland Robert L.,
Musgrove Elizabeth A.
Publication year - 2005
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20690
Subject(s) - cancer research , cyclin dependent kinase 4 , cyclin d , cyclin d1 , cyclin dependent kinase , cell cycle , biology , kinase , carcinogenesis , cyclin a , receptor tyrosine kinase , cyclin , microbiology and biotechnology , breast cancer , tyrosine kinase , cyclin e , cancer , cyclin dependent kinase 2 , signal transduction , protein kinase a , genetics
In breast cancer, cyclins D1 and E and the cyclin‐dependent kinase inhibitors p21 (Waf1/Cip1)and p27 (Kip1) are important in cell‐cycle control and as potential oncogenes or tumor suppressor genes. They are regulated in breast cancer cells following mitogenic stimuli including activation of receptor tyrosine kinases and steroid hormone receptors, and their deregulation frequently impacts on breast cancer outcome, including response to therapy. The cyclin‐dependent kinase inhibitor p16 (INK4A) also has a critical role in transformation of mammary epithelial cells. In addition to their roles in cell cycle control, some of these molecules, particularly cyclin D1, have actions that are not mediated through regulation of cyclin‐dependent kinase activity but may be important for loss of proliferative control during mammary oncogenesis. © 2005 Wiley‐Liss, Inc.