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Carcinogenesis Advance Access published online on April 20, 2009
Carcinogenesis, 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 Current address: Immune Tolerance Institute, San Carlos, CA 94070, USA

* to whom correspondence should be addressed, Tel: 206 667 4252, Fax: 206 667 5815, email: cjkemp{at}fhcrc.org

The cyclin dependent kinase (Cdk) inhibitor p27/Kip1 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 and increased variability in estradiol, 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 estradiol and progesterone. 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.

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


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