Dietary Walnut Suppressed Mammary Gland Tumorigenesis in the C(3)1 TAg Mouse

Walnuts contain multiple ingredients that, individually, have been shown to slow cancer growth, including omega-3 fatty acids, antioxidants, and phytosterols. In previous research, consumption of walnuts has slowed the growth of implanted breast cancers. We wanted to determine whether regular walnut...

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Bibliographic Details
Published inNutrition and cancer Vol. 63; no. 6; pp. 960 - 970
Main Authors Hardman, W. Elaine, Ion, Gabriela, Akinsete, Juliana A, Witte, Theodore R
Format Journal Article
LanguageEnglish
Published Philadelphia, PA Taylor & Francis Group 01.08.2011
Franklin Institute Press
Taylor& Francis
Taylor & Francis Ltd
Taylor & Francis
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Summary:Walnuts contain multiple ingredients that, individually, have been shown to slow cancer growth, including omega-3 fatty acids, antioxidants, and phytosterols. In previous research, consumption of walnuts has slowed the growth of implanted breast cancers. We wanted to determine whether regular walnut consumption might reduce the risk for developing cancer. Homozygous male C(3)1 TAg mice were bred with female SV129 mice consuming either the control AIN-76 diet or the walnut-containing diet. At weaning, the female hemizygous pups were randomized to control or walnut-containing diets and followed for tumor development. Compared to a diet without walnuts, consumption of walnuts significantly reduced tumor incidence (fraction of mice with at least one tumor), multiplicity (number of glands with tumor/mouse), and size. Gene expression analyses indicated that consumption of the walnut diet altered expression of multiple genes associated with proliferation and differentiation of mammary epithelial cells. A comparison with another dietary intervention indicated that the omega 3 content alone did not account for the extent of tumor suppression due to the walnut. The results of this study indicate that walnut consumption could contribute to a healthy diet to reduce risk for breast cancer.
Bibliography:http://dx.doi.org/10.1080/01635581.2011.589959
ISSN:1532-7914
0163-5581
1532-7914
DOI:10.1080/01635581.2011.589959