Journal Article

Induction of the apoptosis-promoting protein Bak by perillyl alcohol in pancreatic ductal adenocarcinoma relative to untransformed ductal epithelial cells.

K R Stayrook, J H McKinzie, Y D Burke, Y A Burke and P L Crowell

in Carcinogenesis

Volume 18, issue 8, pages 1655-1658
Published in print August 1997 | ISSN: 0143-3334
Published online August 1997 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/18.8.1655
Induction of the apoptosis-promoting protein Bak by perillyl alcohol in pancreatic ductal adenocarcinoma relative to untransformed ductal epithelial cells.

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Perillyl alcohol has antitumor activity toward pancreas and other cancers with low toxicity. Here, we have investigated the mechanism of action responsible for the differential sensitivity of malignant versus non-malignant pancreatic cells to the drug. We report that the rate of apoptosis is over 6-fold higher in perillyl alcohol-treated pancreatic adenocarcinoma cells than in untreated cells, and that the effect of perillyl alcohol on pancreatic tumor cells is significantly greater than its effect on non-malignant pancreatic ductal cells. Moreover, the perillyl alcohol-induced increase in apoptosis in all of the pancreatic tumor cells is associated with a 2- to 8-fold increase in the expression of the proapoptotic protein Bak, but Bak expression is not affected by perillyl alcohol in non-malignant cells. Thus, the antitumor activity of perillyl alcohol toward pancreatic cancers may be due to preferential stimulation of Bak-induced apoptosis in malignant versus normal cells. Bak may, therefore, be a useful biomarker for the chemopreventive and therapeutic effects of perillyl alcohol.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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