P53 in the Anticancer Mechanism of Vitamin E

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:    Frankp@chiro.org

FROM:   Eur J Cancer B Oral Oncol 1993 (Oct);   29B (4):   313–318

Schwartz J, Shklar G, Trickler D

Department of Oral Medicine and Oral Pathology,
Harvard School of Dental Medicine,
188 Longwood Avenue,
Boston, Massachusetts 02115, USA

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Immunohistochemical techniques were used to study the expression of "wild type" p53 and "mutant" p53 in experimental cancer inhibition by vitamin E. The cancer model used was the squamous cell carcinoma of hamster buccal pouch induced by the carcinogen 7,12 dimethylbenz(a)anthracene (DMBA). Cancer development was studied sequentially for 8-14 weeks and specimens prepared for histological and immunohistochemical interpretation. Primary antibodies used were monoclonal antibodies for "wild type" and "mutant" p53. Specificity of antibodies was confirmed by flow cytometry. Peroxidase-antiperoxidase staining was used on the tissue specimens. In those animals receiving vitamin E the buccal pouch tumour development was significantly inhibited and there was a notable expression of "wild type" p53. There was also a relative absence of "mutant" p53 in the buccal pouch lesions of animals receiving vitamin E. These observations suggest that vitamin E may inhibit cancer formation by stimulating the expression of a cancer suppressor gene.

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