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Archive - Apr 7, 2011

Soy Increases Radiation’s Ability to Kill Lung Cancer

Components in soybeans increase radiation's ability to kill lung cancer cells, according to a Wayne State University study published in the April 2011 issue of the Journal of Thoracic Oncology, the official monthly journal of the International Association for the Study of Lung Cancer. "To improve radiotherapy for lung cancer, we are studying the potential of natural non-toxic components of soybeans, called soy isoflavones, to augment the effect of radiation against the tumor cells and at the same time protect normal lung cells against radiation injury," said Dr. Gilda Hillman, associate professor in the Department of Radiation Oncology at Wayne State University's School of Medicine and the Karmanos Cancer Institute, who led the team of researchers. "These natural soy isoflavones can sensitize cancer cells to the effects of radiotherapy by inhibiting the survival mechanisms that cancer cells activate to protect themselves," Dr. Hillman said. "At the same time, soy isoflavones can also act as antioxidants, which protect normal tissues against unintended damage from the radiotherapy." Dr. Hillman and her team demonstrated that soy isoflavones increase killing of cancer cells by radiation via blocking DNA repair mechanisms, which are turned on by the cancer cells to survive the damage caused by radiation. Human A549 non-small cell lung cancer (NSCLC) cells that were treated with soy isoflavones before radiation showed more DNA damage and less repair activity than cells that received only radiation. Researchers used a formulation consisting of the three main isoflavones found in soybeans, including genistein, daidzein and glycitein.

Two Metastasis-Promoting Molecules Are Identified

For many types of cancer, the original tumor itself is usually not deadly. Instead, it's the spread of a tiny subpopulation of cells from the primary tumor to other parts of the body—the process known as metastasis—that all too often kills the patient. Now, researchers at Albert Einstein College of Medicine of Yeshiva University have identified two molecules that enable cancer to spread inside the body. These findings could eventually lead to therapies that prevent metastasis by inactivating the molecules. The regulatory molecules are involved in forming invadopodia, the protrusions that enable tumor cells to turn metastatic – by becoming motile, degrading extracellular material, penetrating blood vessels and, ultimately, seeding themselves in other parts of the body. The research appears online on April 7, 2011 in Current Biology. The study's senior author is Dr. John Condeelis, co-chair and professor of anatomy and structural biology, co-director of the Gruss Lipper Biophotonics Center and holder of the Judith and Burton P. Resnick Chair in Translational Research at Einstein. Dr. Condeelis and his team identified two molecules (p190RhoGEF and p190RhoGAP) that regulate the activity of RhoC, an enzyme that plays a crucial role during tumor metastasis and that has been identified as a biomarker for invasive breast cancer. "In vitro as well as in vivo studies have shown that RhoC's activity is positively correlated with increased invasion and motility of tumor cells," said corresponding author Dr. Jose Javier Bravo-Cordero, Ph.D., a postdoctoral fellow in the labs of Dr. Condeelis and assistant professor Louis Hodgson, Ph.D., in the Gruss Lipper Biophotonics Center and the department of anatomy and structural biology.

Vision Loss Slowed in Severe Form of Macular Degeneration

A phase 2 clinical trial for the treatment of a severe form of age-related macular degeneration (AMD) called geographic atrophy (GA) has become the first study to show the benefit of a therapy to slow the progression of vision loss for this disease. The results highlight the benefit of the use of a neurotrophic factor to treat GA and provide hope to nearly one million Americans suffering from GA. The multi-center research team, including Dr. Kang Zhang, of the University of California, San Diego, Shiley Eye Center, the lead author of the paper and one of the leading investigators in the study, found that long-term delivery of ciliary neurotrophic factor (CNTF) served to re-nourish the retina and stop or slow the loss of visual acuity caused by the disorder. The results were published online on March 28, 2011, in PNAS. According to Dr. Zhang -- professor of ophthalmology and human genetics at the UCSD School of Medicine and director of UCSD's Institute of Genomic Medicine – there is currently no effective treatment for dry AMD or GA, though there is a very big need. "This could open the door to long-term treatment of dry AMD, using a simple surgical procedure." AMD is a leading cause of vision loss in Americans age 60 and older. It is a disease that causes cells in the macula – the part of the eye that allows us to see in fine detail – to die. There are two forms of the disorder, wet and dry AMD. GA is considered the end stage of dry AMD, where central vision is lost. According to the National Eye Institute, wet AMD occurs when abnormal blood vessels behind the retina start to grow under the macula. These new blood vessels tend to be very fragile and often leak blood and fluid. The blood and fluid raise the macula from its normal place at the back of the eye, resulting in rapid loss of central version.