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April 20th

Nutlin-3a Activates p53, Stimulates Apoptosis in Glioblastoma Cells

Researchers of Apoptosis and Cancer Group of the Bellvitge Biomedical Research Institute (IDIBELL) have found that a small molecule, Nutlin-3a, an antagonist of MDM2 protein, stimulates the signaling pathway of another protein, p53. In this way, it induces cell death and senescence (loss of proliferative capacity) in brain cancer, a fact that slows the cancer’s growth. These results open the door for MDM2 agonists as new treatments for glioblastomas. The study was published online on April 5, 2011, in the journal PLOS One. Glioblastoma multiforme is the most common brain tumor in adults and the most aggressive. Despite efforts on new treatments and technological innovation in neurosurgery, radiation therapy, and clinical trials of new therapeutic agents, most patients die two years after diagnosis. Dr. Avelina Tortosa, IDIBELL and University of Barcelona (UB) researcher, coordinator of the study, explained that one objective of her group is "to find substances that sensitize tumor cells to radiotherapy for more efficient treatments.” There is evidence that several genetic alterations promote the growth, invasion, and resistance to stimuli that induce programmed cell death (apoptosis). Along these lines, the pilot project TCGA (The Cancer Genome Atlas) has sequenced the genome of up to 25 glioblastomas noting that 14% of patients have an increased expression of MDM2 and 35% had alterations in p53 expression (apoptosis-inducing). That's why research is now focused on the development of new therapeutic strategies that target the apoptosis in gliomas. The aim of this study was to investigate the antitumor activity of Nutlin-3a in cell lines and primary cultures of glioblastoma.

April 7th

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.

April 4th

Genetic Clues to a Major Cause of Kidney Failure

For the first time, researchers have found five regions in the human genome that increase susceptibility to immunoglobulin A (IgA) nephropathy, a major cause of kidney failure worldwide. "The study is unique in identifying the biological pathways that mediate IgA nephropathy, mapping the way for further study that may reveal practical targets for diagnosis and treatment," said Dr. Ali Gharavi, Division of Nephrology at Columbia University in New York City, the principal investigator. "The cause and development of IgA nephropathy is poorly understood. Many biological pathways have been suggested, but none has been conclusive until now," he said. The ongoing genome-wide association study is funded by the National Institutes of Health’s Office of the Director, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and the National Center for Research Resources, under an NIH Challenge Grant. The project is a part of the $10.4 billion provided to NIH through the Recovery Act. Results were published in the April issue of Nature Genetics. Researchers looked at the genes of 3,144 people of Chinese and European ancestry, all of whom have IgA nephropathy. The disease occurs when abnormal IgA antibodies deposit on the delicate filtering portion of the kidney and form tangles. The immune system tries to get rid of the tangles, but the kidneys are caught in the crossfire, further destroying the delicate filters. Worldwide prevalence of IgA nephropathy appears highest in Asia and southern Europe, and is responsible for most cases of kidney failure in those populations. The U.S. prevalence is much lower — up to 10 percent, although Native Americans from New Mexico have reported rates as high as 38 percent. "IgA nephropathy is most common in Asia, intermediate in prevalence in Europeans and rare in Africans.