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Molecular Biology, Pathobiology, and Genetics |
1 Department of Surgery and The Alvin J. Siteman Cancer Center, Washington University School of Medicine, St. Louis, Missouri; 2 Food Research Laboratories, Mitsui Norin Co., Shizuoka, Japan; and 3 Chemoprevention Branch, National Cancer Institute, Bethesda, Maryland
Requests for reprints: Ming You, Department of Surgery and the Alvin J. Siteman Cancer Center, Washington University, Campus Box 8109, 660 South Euclid Avenue, St. Louis, MO 63110. Phone: 314-362-9294; Fax: 314-362-9366; E-mail: youm{at}wustl.edu.
Green tea has been shown to be a potent chemopreventive agent against lung tumorigenesis in animal models. Previously, we found that treatment of A/J mice with either green tea (0.6% in water) or a defined green tea catechin extract (polyphenon E; 2.0 g/kg in diet) inhibited lung tumor tumorigenesis. Here, we described expression profiling of lung tissues derived from these studies to determine the gene expression signature that can predict the exposure and efficacy of green tea in mice. We first profiled global gene expressions in normal lungs versus lung tumors to determine genes which might be associated with the tumorigenic process (TUM genes). Gene expression in control tumors and green teatreated tumors (either green tea or polyphenon E) were compared to determine those TUM genes whose expression levels in green teatreated tumors returned to levels seen in normal lungs. We established a 17-gene expression profile specific for exposure to effective doses of either green tea or polyphenon E. This gene expression signature was altered both in normal lungs and lung adenomas when mice were exposed to green tea or polyphenon E. These experiments identified patterns of gene expressions that both offer clues for green tea's potential mechanisms of action and provide a molecular signature specific for green tea exposure. (Cancer Res 2006; 66(4): 1956-63)
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