Friday, June 3, 2011

Genetically Modified Cancer?

“Many scientists claim that the ingestion of genetically engineered food is harmless. Recent evidence, however, shows that there are potential risks of eating such foods as the new proteins produced in such foods could… contain less isoflavones, an important phytoestrogen present in soybeans, believed to protect women from a number of cancers.” [1] This statement jumped out when reading it as assigned reading for another class. Genetically modified food has been met with much criticism due to its unnatural method of enhancing the rate and efficiency of agriculture. As the quote above proclaims this technology compromises the nutritional value of food and thus elevates our susceptibility to cancer, but can this be scientifically proven?



Phytoestrogens, also known as "dietary estrogens", have similar structure to estrogen and can serve as antagonists. Similar to tamoxifen, these plant-derived hormones block activation of estrogen receptors by binding to the estrogen receptor without eliciting a biological response. With tamoxifen this characteristic enabled the drug to be prescribed to breast cancer patients and patients at risk for breast cancer. To determine if phytoestrogens can be another form of cancer treatment, women diagnosed with endometrial cancer were split into three groups. These groups were assigned dietary intake of a class of phytoestrogens: isoflavone, coumestan and lignan. At the end of the trial, they found that women in the isoflavone and lignan groups inversely related to the risk of endometrial cancer. Since phytoestrogen is a hormone, there were different results among postmenopausal and premenopausal women: postmenopausal women who consumed more phytoestrogens had a higher reduced risk of endometrial cancer than premenopausal women. How does this phytochemical function? Attempts to prove efficacy of phytoestrogen as a chemoprevention treatment explain how diets affect our health. Normal mammary epithelial cells and estrogen receptor negative mammary epithelial cells were treated with phytoestrogens and cell growth was measured by cell proliferation [2]. They found after 72hrs of treatment, cell growth was inhibited which was attributed to the induced morphology of cells. The study found that treatment of phytoestrogen increased level of active p53 and p21, which as we know are tumor suppressors, in both cell types. The paper sought to prove that phytoestrogens can act as treatment options for patients with estrogen receptor negative tumors which it succeeds in doing so. However, wouldn’t the reduction of cell growth in normal cells result in a cancer that has a defect in the function of normal tumor supressors? Application of phytoestrogen can not identify the distinction between normal breast cells and estrogen receptor negative breast cells.

Loss of abundance of isoflavones in genetically modified crops such as corn does not necessarily cause cancer; it just diminishes ones ability to reduce their risk of cancer. Even then, reducing amount of isoflavones in our diet is not threatening since it can be obtained from numerous sources: soybean, tofu, tea, vegetables and the skin of many fruits. In fact, isoflavones are not the only phytochemical to exhibit a correlation between intake and reduced risk of cancer. Resveratol is proven to be a promosing candidate for hormone replacement therapy and chemoprevention in breast cancer patients [3].
Consuming more genetically modified corn may substitute the amount of isoflavones missing in one ear of corn. Due to the lack of research on genetically modified organisms, there has not been a significant correlation between intake of genetically modified crops and cancer. Therefore, individuals should continue to eat fruits and vegetables.
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[1] Altieri, Miguel and Peter Rosset. (1999) “Ten Reasons Why Biotechnology will not Ensure Food Security, Protect the Environment and Reduce Poverty in the Developing World” AgBioForum, 2: 3 & 4 pg155-162.
[2] Seo, H., Ju, J., Jang, K, & Shin, I. (2011) “Induction of apoptotic cell death by phytoestrogens by up-regulating the levels of phosphor-p53 and p21 in normal and malignant estrogen receptor α-negative breast cells” Nutrition Research. 31, 139-146.
[3]Sakamoto, T., Horiguchi, H., Oguma, E., & Kayama, F. (2009) “Effects of diverse dietary phytoestrogens on cell growth, cell cycle and apoptosis in estrogen-receptor-positive breast cancer cells” Journal of Nutritional Biochemistry. 21, 856-864.