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Archive - May 5, 2013 - Page

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Genetics of Pulmonary Fibrosis

Researchers from the University of Colorado Denver and colleagues have carried out a genome-wide association study to identify susceptibility loci for fibrotic idiopathic pneumonia. Their results sugget that genes involved in host defense, cell-cell adhesion, and DNA repair contribute to risk for this disease. Specifically, the scientists confirmed association with TERT at 5p15, MUC5B at 11p15, and the 3q26 region near TERC. In addition, they identified seven newly associated loci: FAM13A at 4q22, DSP at 6p24, OBFC1 at 10q24, ATP11A at 13q34,DPP9 at 19p13, and chromosomal regions 7q22 and 15q14-15. The results of this study were published online in Nature Genetics on April 14, 2013. [Nature Genetics abstract]

Why Dense Breasts Predispose to Metastasis in Breast Cancer

Researchers at Washington University School of Medicine in St. Louis have discovered why breast cancer patients with dense breasts are more likely than others to develop aggressive tumors that spread. The finding opens the door to drug treatments that may prevent metastasis. It has long been known that women with denser breasts are at higher risk for breast cancer. This greater density is caused by an excess of a structural protein called collagen. "We have shown how increased collagen in the breasts could increase the chances of breast tumors spreading and becoming more invasive," says Gregory D. Longmore, M.D., professor of medicine. "It doesn't explain why women with dense breasts get cancer in the first place. But once they do, the pathway that we describe is relevant in causing their cancers to be more aggressive and more likely to spread." The results were published online on May 5, 2013 in Nature Cell Biology. Working in mouse models of breast cancer and with breast tumor samples from patients, Dr. Longmore and his colleagues showed that a protein that sits on the surface of tumor cells, called DDR2, binds to collagen and activates a multi-step pathway that encourages tumor cells to spread. "We had no idea DDR2 would do this," says Dr. Longmore, also professor of cell biology and physiology. "The functions of DDR2 are not well understood, and it has not been implicated in cancer -- and certainly not in breast cancer -- until now.” At the opposite end of the chain of events initiated by DDR2 is a protein called SNAIL1, which has long been associated with breast cancer metastasis. Dr. Longmore and his colleagues found that DDR2 is one factor helping to maintain high levels of SNAIL1 inside a tumor cell's nucleus, a necessary state for a tumor cell to spread.

Epileptic Seizures Halted in Mouse Model

University of California San Francisco (UCSF) cell therapy raises hope for severe human forms of epilepsy. UCSF scientists controlled seizures in epileptic mice with a one-time transplantation of medial ganglionic eminence (MGE) cells, which inhibit signaling in overactive nerve circuits, into the hippocampus, a brain region associated with seizures, as well as with learning and memory. Other researchers had previously used different cell types in rodent cell transplantation experiments and failed to stop seizures. Cell therapy has become an active focus of epilepsy research, in part because current medications, even when effective, only control symptoms and not underlying causes of the disease, according to Scott C. Baraban, Ph.D., who holds the William K. Bowes Jr. Endowed Chair in Neuroscience Research at UCSF and led the new study. In many types of epilepsy, he said, current drugs have no therapeutic value at all. "Our results are an encouraging step toward using inhibitory neurons for cell transplantation in adults with severe forms of epilepsy," Dr. Baraban said. "This procedure offers the possibility of controlling seizures and rescuing cognitive deficits in these patients." The findings, which are the first ever to report stopping seizures in mouse models of adult human epilepsy, were published online on May 5, 2013 in Nature Neuroscience. During epileptic seizures, extreme muscle contractions and, often, a loss of consciousness can cause seizure sufferers to lose control, fall, and sometimes be seriously injured. The unseen malfunction behind these effects is the abnormal firing of many excitatory nerve cells in the brain at the same time.