Ji Su Park and Dr. Merrill Christensen, Department of Nutrition, Dietetics, and Food Science
Prostate cancer is the most frequently diagnosed cancer and the second leading cause of cancer deaths in American men, with a predicted 29,720 deaths in 2013. (1) Previous studies have shown that both selenium (Se) and soy isoflavones reduce risk for prostate cancer when consumed at high levels. (2-3) However, little is known about the effect of Se and isoflavones combined on cancer progression or whether it matters when these supplements are introduced into the diet to decrease cancer progression. In this study, we investigated the individual and combinational effects of Se and soy and the role of timing of supplementation on the progression of prostate cancer in the TRAMP (Transgenic Adenocarcinoma of the Mouse Prostate) mouse model.
I successfully completed my part of this project to the best of my ability and given the circumstances and timeline of the project. However, the project will still continue for completion of examination and statistical analysis of the rest of the 18 and 24-week animals.
During my time in the Christensen lab, our team of researchers was able to harvest the prostate tissues and tumor samples of 18-week animals and stained them with Hematoxylin and Eosin. We scored the prostate tissues for the 18-week animals based on a 1-6 scale of the human Gleason scoring system, as adapted by Greenberg et al. (4) with 1 being normal, well differentiated tissue, and 6 being the most advanced, poorly differentiated adenocarcinoma.
However, different scores may be represented in the same tissue section (e.g. in one tissue, there may be both 3’s and 5’s present), which presented an issue for statistical analysis of the obtained scores. Therefore, our team adapted a new way of making the H&E scores more statistically quantifiable. We estimated what percentage of each tissue section, examined microscopically, was involved in each lesion (e.g. 20% of a tissue section scored “1”, 50% scored “2”, 20% scored “3”, and 10% scored “4”). A single score for each tissue section was obtained by multiplying each lesion number by the percentage of its involvement in that tissue section, then summing the products. Each tissue was scored by at least 3 blinded student researchers and the mean score was used for statistical analysis. So far, we were able to run analysis on the 12-week animal tissues only.
With the data and analysis that we have so far, we are able to conclude that dietary supplementation of Se was correlated with a lower histology score in the 12-week animals, which suggests a chemopreventive effect of Se on the progression of prostate cancer. However, the earlier timing of supplementation of the high isoflavone, high Se diet was not shown to be significantly correlated with lower histology scores in the 12-week animals. It is not yet conclusive as we are still anticipating data from the 18 and 24-week animals, but we expect that the animals started on the high isoflavone, high Se diet will be correlated with lower histology scores.
Presentation of Findings
Our findings from the 12-week animals were presented in a poster at the Utah Conference of Undergraduate Research in February 2013 at Utah State University.
- American Cancer Society. Prostate Cancer Key Statistics 2013. [updated 2013; cited February 2013]; Available from: http://www.cancer.org/cancer/prostatecancer/detailedguide/prostate-cancer-key-statistics
- Duffield-Lillico AJ, Dalkin BL, Reid ME, Turnbull BW, Slate EH, Jacobs ET, et al. Selenium supplementation, baseline plasma selenium status and incidence of prostate cancer: an analysis of the complete treatment period of the Nutritional Prevention of Cancer Trial. BJU Int. 2003;91(7):608-12.
- Sonoda T, Nagata Y, Mori M, Miyanaga N, Takashima N, Okumura K, et al. A case-control study of diet and prostate cancer in Japan: possible protective effect of traditional Japanese diet. Cancer science. 2004;95(3):238-42.
- Greenberg NM, Foster BA, et al. Pathobiology of Autochthonous Prostate Cancer in a Pre-Clinical Transgenic Mouse Model. The Prostate. 2003;55:219-237.