Cancer Research:
Vitamin E and Tumor Growth
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When microbiologists grow cultures of bacteria or other single-cell organisms, the cells typically grow and divide very rapidly. The common laboratory bacterium E. coli, for example, can divide as rapidly as three times per hour when conditions are favorable. In many-celled organisms like ourselves, however, such proliferation of cells would be disastrous. While some types of cells, like the cells that line the digestive tract, do divide fairly frequently, no cell is allowed to divide uncontrollably--under normal circumstances. When the control of cell division fails, the aberrant cell and its offspring form an abnormal mass we call a tumor. More rarely, the tumor becomes mobile, capable of migrating out of the tissue where it originated, potentially invading other parts of the body. This is the dreaded condition we call metastatic cancer. Molecular biologists have made enormous advances in understanding the complex processes of cancer and, as a result, are beginning to understand the subtle ways that the division of normal cells is controlled. When cells are growing and dividing, they proceed through orderly cell cycles. In each cycle, the cell grows; the DNA in the cell's chromosomes is duplicated; and eventually the cell divides into two daughter cells. In normal cells, the timing of the cell cycle is controlled in part by chemical signals called growth factors that diffuse through the cells' watery environment. The growth factors transmit signals within the cells to direct the progress of the cell cycle. In most mature tissues, growth factors also serve to halt the cell cycle to prevent proliferation of unnecessary cells. Damaged cells, or cells that have exceeded some predetermined life span, may be instructed not only to stop dividing but even to "commit suicide" by fragmenting their chromosomes. Cancer cells are formerly normal cells that have escaped orderly control of either their cell cycle or life span. For reasons that scientists are still seeking to understand, these damaged cells do not respond to instructions to destroy themselves. 
The mechanisms controlling cell proliferation are extremely complex. Karen Heim, a doctoral graduate student in Biological Sciences at The University of Texas at Austin, is one of several researchers examining the role of vitamin E succinate (VES) in regulating human tumor cells. Heim is associated with the laboratories of UT molecular genetics professor Bob G. Sanders and nutritional sciences professor Kimberly Kline. These collaborating laboratories investigate the effects of fat-soluble vitamins on tumor growth. Vitamin E, like some other vitamins, is an antioxidant: it protects cellular proteins and DNA from damage from highly reactive forms of oxygen. However, Heim points out that vitamin E succinate, a derivative of vitamin E, is not an antioxidant, but affects tumor development in a very different way. (Vitamin E succinate is not the most common form of the vitamin found in commercial dietary supplements, but it is available in a few brands.) Heim studies the effects of VES on a specific type of cell originally derived from human breast cancers and cultured in the laboratory. Other graduate students in the group examine the effects of VES on other types of cancer cells and study the ways VES controls tumor growth. Because VES acts on tumors from different tissues, Heim notes, future medical applications of VES may be in cancer prevention as well as in treatment of certain types of established tumors. However, such applications must await further research. Although VES inhibits the growth of cancer cells in laboratory cultures, its efficacy against cancers in humans is not yet established. By Jack Kent, Jr.,
Other UT Research on VES and CancerSeveral UT graduate students in the Sanders and Kline research groups are investigating the role of vitamin E succinate (VES) in tumor regulation. Karen Israel has observed effects of VES on cultured prostate cancer cells that parallel the effects on breast cancer cells studied by Heim. In the prostate cancer cells, VES halts DNA synthesis and induces cell death (apoptosis), indicating that VES is effective against more than one kind of cancer. Israel's studies show that VES triggers apoptosis in prostate cancer cells via a cell membrane receptor called Fas. When activated, Fas initiates a cascade of events that eventually results in the systematic degradation of the tumor cells. Lisa Hotchkiss investigates changes in gene expression in cells treated with VES. Certain messenger RNAs--the intermediate information molecules that carry the code for synthesis of new proteins--increase or decrease in abundance in cancer cells after VES treatment. Characterization of these mRNAs and the proteins that they encode will clarify the mechanism of VES action on tumor cells. Kristin Anderson studies how VES is taken up and metabolized by cancer cells, with the goal of understanding why this form of Vitamin E is an effective anticancer agent. VES causes cancer cells to differentiate, or become more like specific tissue cells, prior to apoptosis. Huihong You examines chemical markers of the differentiation process in human breast cancer cells treated with VES. Karla Lawson examines the effectiveness of VES in preventing or treating breast cancer. Professor Kimberly Kline (Nutritional Sciences, Department of Human Ecology) has devoted much of her research career to investigating the multiple effects of vitamin E and its derivatives (including VES) on cancer development and growth. Professor Bob G. Sanders (Section of Molecular Genetics and Microbiology, School of Biological Sciences) conducts research that includes cancer biology and immune deficiencies caused by retroviruses. By Jack Kent, Jr.,
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