Journal Article

Endocrine dysfunction in p27<sup>Kip1</sup> deficient mice and susceptibility to <i>Wnt-1</i> driven breast cancer

Cynthia E. Glover, Kay E. Gurley, Kyung-Hoon Kim, Barry Storer, Mathew L. Fero and Christopher J. Kemp

in Carcinogenesis

Volume 30, issue 6, pages 1058-1063
Published in print June 2009 | ISSN: 0143-3334
Published online April 2009 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgp089
Endocrine dysfunction in p27Kip1 deficient mice and susceptibility to Wnt-1 driven breast cancer

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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.

Journal Article.  4122 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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