The active components of PC-SPES are unknown. Laboratory analysis of PC-SPES by HPLC, gas chromatography, and mass spectrometry indicate the presence of estrogenic organic compounds different from diethylstilbestrol (DES), estrone, and estradiol. In vitro testing of this extract shows suppressed cell proliferation and reduced clonogenicity in human tumor cell lines, including prostrate, breast, and colon. The predominant cell cycle effect induced by PC-SPES is prolongation of G1 phase; however, apoptosis was observed after exposure of tumor cells to PC-SPES for 48 hours or longer. PC-SPES also inhibits proliferation of LNCaP prostate cell lines, associated with a 60-70% down regulation of the proliferating cell nuclear antigen. Preliminary studies evaluating the viability of prostate cancer cell lines LNCaP, LNCaP apoptosis-resistant derivative, LNCaP-bcl-2, PC3, and DU145 at three concentrations of PC-SPES show inhibited growth at concentrations of 4 mcg/ml or less. Another recent in vitro study indicates its cytotoxicity may be due to alteration of expression of specific genes involved in regulating the cell cycle, cell structure and androgen response. No single botanical or chemical extract appears responsible for the overall effects of this product. PC-SPES has been found to contain small amount of diethylstibestrol and ethinyl estradiol. It is unclear whether these agents account for its anticancer effects.
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