QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kavanaugh, C. Articles by Green, J. E. Search for Related Content PubMed PubMed Citation Articles by Kavanaugh, C. Articles by Green, J. E.

---

Supplement: Nutritional Genomics and Proteomics in Cancer Prevention

The Use of Genetically Altered Mice for Breast Cancer Prevention Studies¹

Claudine Kavanaugh^*, and Jeffrey E. Green^*,2

^* Laboratory of Cellular Regulation and Carcinogenesis, National Cancer Institute, Bethesda, MD and Division of Preventive Oncology, Cancer Prevention Fellowship Program, National Cancer Institute, Bethesda, MD 20892

² To whom correspondence should be addressed. E-mail: jegreen{at}nih.gov.

Chemoprevention through nutritional and dietary changes may offer an important means of inhibiting the development and progression of breast cancer, which would have a major impact on public health. Studies to assess the efficacy of potential chemopreventive compounds are difficult to perform in large human populations, whereas the use of genetically engineered mice (GEM) for preclinical testing offers several advantages. GEM models can be utilized to assess the inhibitory effects of nutritional and chemopreventive agents on well-defined oncogenic signaling pathways. Because several transgenic mouse models progress through a well-defined temporal series of stages leading to invasive carcinoma formation, they may be particularly useful for determining cancer stage-specific responses to nutritional and chemopreventive agents. The C3(1)SV40 T/t-antigen transgenic mouse mammary cancer model has been utilized for chemopreventive research in which mammary tumors develop over a well-characterized time course. Several compounds have been shown to inhibit mammary tumor development in this model, including retinoids, di-fluoromethylornithine (DFMO), dehydroepiandrosterone (DHEA), antiangiogenic compounds and nonsteroidal antiinflammatory drugs (NSAID). All of the chemopreventive agents used in the C3(1)Tag mammary mouse model appear to affect the promotion stage of tumorigenesis, suggesting that these agents may be useful in inhibiting the transition of human ductal carcinoma in situ (DCIS) to invasive carcinoma. Selective combinations of chemopreventive agents may be particularly useful for targeting multiple signaling pathways involved in cancer development and progression leading to improved clinical responses. The application of gene expression profiling to chemopreventive studies will aid in the selection of appropriate models for preclinical testing and further define mechanisms of action.

KEY WORDS: • genetically engineered mice • chemoprevention • breast cancer

This article has been cited by other articles:

				X. Zhang, R. G. Mehta, D. D. Lantvit, K. T. Coschigano, J. J. Kopchick, J. E. Green, S. Hedayat, K. T. Christov, V. H. Ray, T. G. Unterman, et al. Inhibition of estrogen-independent mammary carcinogenesis by disruption of growth hormone signaling Carcinogenesis, January 1, 2007; 28(1): 143 - 150. [Abstract] [Full Text] [PDF]

				D. E. Malarkey, J. S. Parker, C. A. Turman, A. M. Scott, R. S. Paules, J. Collins, and R. R. Maronpot Microarray Data Analysis of Mouse Neoplasia Toxicol Pathol, January 1, 2005; 33(1): 127 - 135. [Abstract] [Full Text] [PDF]

				C. K. Abbey, A. D. Borowsky, E. T. McGoldrick, J. P. Gregg, J. E. Maglione, R. D. Cardiff, and S. R. Cherry In vivo positron-emission tomography imaging of progression and transformation in a mouse model of mammary neoplasia PNAS, August 3, 2004; 101(31): 11438 - 11443. [Abstract] [Full Text] [PDF]