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 Kline, K. Articles by Sanders, B. G. Search for Related Content PubMed PubMed Citation Articles by Kline, K. Articles by Sanders, B. G.

---

Supplement: International Research Conference on Food, Nutrition, and Cancer

Vitamin E and Breast Cancer¹

Division of Nutrition and School of Biological Sciences, University of Texas at Austin, Austin, TX 78712

²To whom correspondence should be addressed. E-mail: k.kline{at}mail.utexas.edu.

Vitamin E is a term that describes a group of compounds with similar yet unique chemical structures and biological activities. One interesting property possessed by certain vitamin E compounds—namely, -tocotrienol, RRR--tocopheryl succinate [vitamin E succinate (VES), a hydrolyzable ester-linked succinic acid analogue of RRR--tocopherol], and a novel vitamin E analogue referred to as -TEA (-tocopherol ether linked acetic acid analogue, which is a stable nonhydrolyzable analogue of RRR--tocopherol)—is their ability to induce cancer cells but not normal cells to undergo a form of cell death called apoptosis. In contrast, the parent compound, RRR--tocopherol, also referred to as natural or authentic vitamin E and known for its antioxidant properties, does not induce cancer-cell apoptosis. Efforts to understand how select vitamin E forms can induce cancer cells to undergo apoptosis have identified several nonantioxidant biological functions, including restoration of pro-death transforming growth factor-ß and Fas signaling pathways. Recent studies with -TEA show it to be a potent inducer of apoptosis in a wide variety of epithelial cancer cell types, including breast, prostate, lung, colon, ovarian, cervical, and endometrial in cell culture, and to be effective in significantly reducing tumor burden and metastasis in a syngeneic mouse mammary tumor model, as well as xenografts of human breast cancer cells. Studies also show that -TEA, in combination with the cyclooxygenase-2 inhibitor celecoxib and the chemotherapeutic drug 9-nitro-camptothecin decreases breast cancer animal model tumor burden and inhibits metastasis significantly better than do single-agent treatments.

KEY WORDS: • vitamin E • cancer • chemotherapy • tumor burden • metastasis

This article has been cited by other articles:

				T.-C. HSIEH and J. M. WU Targeting CWR22Rv1 Prostate Cancer Cell Proliferation and Gene Expression by Combinations of the Phytochemicals EGCG, Genistein and Quercetin Anticancer Res, October 1, 2009; 29(10): 4025 - 4032. [Abstract] [Full Text] [PDF]

				Y. Cui, J. M Shikany, S. Liu, Y. Shagufta, and T. E Rohan Selected antioxidants and risk of hormone receptor-defined invasive breast cancers among postmenopausal women in the Women's Health Initiative Observational Study Am. J. Clinical Nutrition, April 1, 2008; 87(4): 1009 - 1018. [Abstract] [Full Text] [PDF]