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Archive - Feb 22, 2012

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Study Suggests Novel Genetic Model of Skin Cancer

The University of Kentucky (UK) has announced that Dr. Daret St. Clair, the James Graham Brown Endowed Chair and professor of toxicology, has published the first comprehensive study that provides insight into the relationship between two types of suppressors in cancerous tumors. The results will enhance the understanding of transcriptional mechanisms in carcinogenesis. The study was supported by a National Cancer Institute research grant and was published in the November 1, 2011 issue of Cancer Research. Dr. St. Clair and her team generated transgenic mice expressing a luciferase reporter gene under the control of human MnSOD promoter-enhancer elements and investigated the changes of MnSOD transcription using the 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-l3-acetate (TPA) multistage skin carcinogenesis model. Manganese superoxide dismutase (MnSOD) plays a critical role in the survival of aerobic life, and its abnormal expression has been implicated in carcinogenesis and tumor resistance to therapy. Despite extensive studies in MnSOD regulation and its role in cancer, when and how the alteration of MnSOD expression occurs during the process of tumor development in vivo are unknown. The current results show that MnSOD expression was suppressed at a very early stage, but increased at late stages of skin carcinogenesis. The suppression and subsequent restoration of MnSOD expression were mediated by two transcription factors, Sp1 and p53. Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal appearing skin and benign papillomas. In squamous cell carcinomas, Sp1 binding increased due to loss of functional p53. Dr. St.

Potentially Deadly Fungus Senses Body’s Defenses to Evade Them

Dr. Glen Palmer, Assistant Professor of Microbiology, Immunology & Parasitology at Louisiana State University (LSU) Health Sciences Center New Orleans, was part of an international research team led by Dr. Luigina Romani, at the University of Perugia in Italy, that discovered opportunistic fungi like Candida albicans can sense the immune status of host cells and adapt, evading immune system defenses. Unlike previous studies, this research investigated both sides of the infection equation, as well as the interaction between the fungi and the cells they will invade. The findings were published online on February 21, 2012 in Nature Communications. This study demonstrates that this process is much more elaborate and complex than previously understood. The researchers determined that C. albicans binds to the host immune signaling molecule, interleukin (IL) 17A, which permits the fungus to navigate and tolerate the active immune environment of healthy host tissue, mounting effective countermeasures. IL-17A may also contribute to disease susceptibility by modifying the intrinsic virulence of the fungus. This study provides molecular evidence that by exploiting IL-17A, the fungus not only survives, but can cause disease to develop. "It's a bit like the fungus is listening in to the conversations our immune system is having so it can best determine how to react and survive in our tissues. This may also be a crucial step in determining when this opportunist decides to invade host tissue and cause life-threatening disease in an immunosuppressed patient," notes Dr. Palmer. According to the Centers for Disease Control and Prevention, there are more than 20 species of Candida yeasts that can cause infection in humans, the most common of which is Candida albicans.