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Carcinogenesis Advance Access originally published online on April 20, 2009
Carcinogenesis 2009 30(6):1058-1063; doi:10.1093/carcin/bgp089
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Endocrine dysfunction in p27Kip1 deficient mice and susceptibility to Wnt-1 driven breast cancer

Cynthia E. Glover1,2, Kay E. Gurley1, Kyung-Hoon Kim1,3, Barry Storer1, Mathew L. Fero1 and Christopher J. Kemp1,*

1 Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
2 SNBL, USA. Ltd, Everett, WA 98203, USA
3 Present address: Immune Tolerance Institute, San Carlos, CA 94070, USA

* To whom correspondence should be addressed. Tel: +1 206 667 4252; Fax: +1 206 667 5815; Email: cjkemp{at}fhcrc.org

The cyclin-dependent kinase (Cdk) inhibitor p27Kip1 (p27) is a marker of prognosis in many cancers, including breast cancer. Low p27 expression correlates with poor prognosis, especially in hormone receptor positive breast tumors. This association suggests a role for p27 in hormone-dependent cancer. We used the Wnt-1 transgenic mouse model to further explore the role of p27 in hormone-driven breast cancer. We found that p27 deficiency did not alter breast cancer rate in either male or female Wnt-1 mice. However, we did find p27–/– females had reduced levels of serum progesterone (P) and increased variability in estradiol (E), which could have affected their cancer susceptibility. To equalize hormone levels, an additional cohort of Wnt-1 female mice was ovariectomized and implanted with slow release pellets of E and P. Although this treatment did not alter the breast cancer rate, it did accelerate the development of pituitary and gastric tumors in p27–/– mice. This study shows that while not a significant inhibitor of Wnt-1-driven breast cancer, p27 inhibits gastric tumors, whose latency is modulated by sex steroids.

Abbreviations: Cdk, cyclin-dependent kinase; E, estradiol; ER, estrogen receptor; OVX, ovariectomy; p27, p27Kip1; P, progesterone

Received December 5, 2008; revised March 11, 2009; accepted April 7, 2009.


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