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Archive - Apr 12, 2011

Loss of Cell Adhesion Protein Drives Oral/Esophageal Cancers in Mice

Squamous cell cancers of the oral cavity and esophagus are common throughout the world, with over 650,000 cases of oral cancer each year and esophageal cancer representing the sixth most common cause of cancer death in men. Research by University of Pennsylvania School of Medicine investigators has shown that a protein that helps cells stick together is frequently absent or out of place in these cancers, but it's unclear if its loss causes the tumors. The investigators report that mice engineered to lack this protein, called p120-catenin (p120ctn), in the oral-upper digestive tract develop squamous cell cancers. The data, reported in the April 12, 2011 issue of Cancer Cell, settles a 20-year debate and proves that p120ctn is a tumor-suppressor protein. What's more, the tumors that form in this mouse model closely resemble human disease and may point the way to novel therapies and early detection strategies. "As the mice aged, what we saw was a dramatic evolution of precancer to cancer," says senior author Dr. Anil K. Rustgi, the T. Grier Miller Professor of Medicine and Genetics and chief of Gastroenterology. "Both the precancerous growth, called dysplasia, and the cancer look exactly like what we see in humans. This is really exciting because it supports efforts for prevention and early detection, especially in people who drink alcohol and smoke cigarettes excessively and are at high risk for the disease in many regions of the world." In healthy tissues, p120ctn is part of a protein complex that holds epithelial cells in tightly packed sheets. When p120ctn (or another of these cell adhesion proteins) is lost, a wide variety of cancers, including those in prostate, breast, pancreas, colon, skin, bladder, and the endometrium, can result.

Discovery of Two Genes May Aid Battle Against Staph Aureus

The discovery of two genes that encode copper- and sulfur-binding repressors in the hospital terror Staphylococcus aureus means two new potential avenues for controlling the increasingly drug-resistant bacterium, scientists say in the April 15, 2011 issue of the Journal of Biological Chemistry. "We need to come up with new targets for antibacterial agents," said Indiana University Bloomington biochemist Dr. David Giedroc, who led the project. "Staph is becoming more and more multi-drug resistant, and both of the systems we discovered are promising." The work was a collaboration of members of Giedroc's laboratory, and those of Vanderbilt University School of Medicine infectious disease specialist Dr. Eric Skaar, and University of Georgia chemist Dr. Robert Scott. MRSA, or multidrug-resistant Staphylococcus aureus, is the primary cause of nosocomial infections in the United States. About 350,000 infections were reported last year, about 20 percent of which resulted in fatalities, according to the Centers for Disease Control. One to two percent of the U.S. population has MRSA in their noses, a preferred colonization spot. One of the repressors the scientists discovered, CsoR (copper-sensitive operon repressor), regulates the expression of copper resistance genes, and is related to a CsoR previously discovered by the Giedroc group in Mycobacterium tuberculosis, the bacterium that causes tuberculosis in humans. When the bacterium is exposed to excess copper, the repressor binds copper (I) and falls away from the bacterial genome to which it is bound, making it possible for the copper resistance genes to be turned on.

Pigeons Can Recognize Human Faces and Emotions

A study published by two University of Iowa researchers in the March 31, 2011 issue of the Journal of Vision found that pigeons recognize a human face's identity and emotional expression in much the same way as people do. Pigeons were shown photographs of human faces that varied in the identity of the face, as well as in their emotional expression -- such as a frown or a smile. In one experiment, pigeons, like humans, were found to perceive the similarity among faces sharing identity and emotion. In a second, key experiment, the pigeons' task was to categorize the photographs according to only one of these dimensions and to ignore the other. The pigeons found it easier to ignore emotion when they recognized face identity than to ignore identity when they recognized face emotion, according to Dr. Ed Wasserman, Stuit Professor of Experimental Psychology, and graduate student Fabian Soto, both of the UI College of Liberal Arts and Sciences Department of Psychology. "This asymmetry has been found many times in experiments with people and it has always been interpreted as the result of the unique organization of the human face processing system." Soto said. "We have provided the first evidence suggesting that this effect can arise from perceptual processes present in other vertebrates. The point of the project is not that pigeons perceive faces just as we do or that people do not have specialized processes for face perception. Rather, the point is that both specialized and general processes are likely to be involved in peoples' recognition of faces and that the contributions of each should be carefully determined empirically," he added. In fact, the findings could make scientists reconsider their assumptions about how uniquely human cognitive processes might interact with more general processes in complex tasks such as face recognition.

How Anti-Depressants Make New Brain Cells

For the first time in a human model, scientists have discovered how anti-depressants make new brain cells. This implies that researchers can now develop better and more efficient drugs to combat depression. Previous studies have shown that anti-depressants make new brain cells, however, until now it was not known how they did it. In a study published online on April 12, 2011, in the journal Molecular Psychiatry, researchers from the Institute of Psychiatry, King's College London, show that anti-depressants regulate the glucocorticoid receptor (GR) - a key protein involved in the stress response. Moreover, the study shows that all types of anti-depressant are dependent on the GR to create new cells. Depression is expected to be the second leading burden of disease worldwide by the year 2020. Recent studies have demonstrated that depressed patients show a reduction in a process called ‘neurogenesis,’ that is, a reduction in the development of new brain cells. This reduced neurogenesis may contribute to the debilitating psychological symptoms of depression, such as low mood or impaired memory. With as much as half of all depressed patients failing to improve with currently available treatments, developing new effective anti-depressant treatment still remains a great challenge, which makes it crucial to identify new potential mechanisms to target. The Laboratory of Stress, Psychiatry and Immunology (SPI-lab) at King's has been looking into the role of the GR in depression for a number of years. In this study, scientists used human hippocampal stem cells, the source of new cells in the human brain, as a new model to investigate, 'in a dish,' the effects of anti-depressants on brain cells.