ScienceCache

Vol. 188
Dec. 8, 2004

FORM OF CANCER MAY BE TARGET FOR DIABETES DRUGS
In laboratory tests on multiple myeloma cells, researchers have found that this type of cancer expresses a protein that makes it an easy target for an existing class of diabetes drugs. After more investigation, they hope the discovery will lead to a new, targeted therapy for myeloma patients. “To our knowledge, this is the first time anyone has shown that multiple myeloma cells are sensitive to these agents, and we found multiple myeloma cells are killed quite effectively,” says lead author Richard P. Phipps, professor of environmental medicine and of oncology. The drugs in question are from the thiazolidinedione (TZD) class of anti-diabetic therapies, known as PPAR-gamma ligands. They bind to PPAR-gamma, a protein associated with multiple myeloma and many other cancers, as well as chronic inflammation and diabetes. When the drugs bind to PPAR-gamma, at least in laboratory experiments, the cancerous cells are destroyed. PPAR-ligands are emerging as a new type of cancer therapy because they directly target errant cells and stop tumor growth in animal models. Co-investigator Steven Bernstein, who treats myeloma patients at the James P. Wilmot Cancer Center, is cautious but hopeful about the prospects of this research leading to a new treatment. “Although we are optimistic about these early findings, we need to do further investigation to understand how the TZD class of drugs work against multiple myeloma, before clinical trials are warranted.” The research was reported in the November issue of Clinical Immunology.
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‘ SLOW LIGHT’ RESEARCH SPEEDS UP WITH $6.5 MILLION GRANT
Optical computers have long held the promise of incredible computing power, and now researchers are getting a chance to show how some of their work, like bringing light to a near halt, can carry that promise to fruition. The project is spurred on by a Defense Advanced Research Projects Agency (DARPA) award for $6.5 million over the next four and a half years; the project is led by University of Rochester scientists and includes researchers from several other universities as well. “We’ve got an all-star team tackling some of the toughest problems in all-optical processing,” says Robert Boyd, professor of optics and physics, who is leading the effort. In recent work, Boyd and colleagues have developed a system to slow the speed of light to a comparative crawl. Whereas electrical signals have proven simple to store, light wants to race along at speeds up to 186,000 miles per second. Boyd’s system, relatively simple compared to other slow-light systems, puts the brakes on the photons, slowing them to just 127 miles per hour – 5.3 million times slower than light’s normal speed. Such work aimed at controlling light precisely would be crucial to all-optical signal processing, which offers great advantages over today’s techniques. The telecommunications industry, for instance, shuttles tremendous amounts of data via fiber optics, but must convert most of it back and forth to the electrical domain in order to route or process it. A more efficient method would be to process the incoming photons directly, operating at the speed of light and without suffering the inefficiencies associated with the conversion from optical to electrical and back to optical.
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SCIENTISTS ALIGN BILLION-YEAR-OLD PROTEIN WITH EMBRYONIC HEART DEFECTS
Scientists studying a vital protein called Serum Response Factor (SRF) in mice have learned new and unexpected facts about SRF’s role in early cardiovascular development, and how a defect in this gene may be an underlying cause in human miscarriages. The research is reported in this week’s Proceedings of the National Academy of Sciences. At this point it is unclear whether subtle defects in SRF might also be linked to adult cardiovascular disease. However, the research provides a foundation for understanding how gene mutations may disrupt heart function, perhaps making some adults more susceptible to heart failure or irregular reactions to drugs. “One reason for studying the biology of our genetic blueprint is so that we can understand how mutations in the genes encoding for proteins such as SRF may relate to human disease,” says Joseph M. Miano, associate professor of medicine in the Center for Cardiovascular Research. “Defining the full spectrum of genetic mutations is key to genetic screening and gene-based therapies.” SRF is one of nature’s oldest proteins and is essential for life because it supports the basic internal structure of all living cells. Its function is to carefully turn on 300 of our approximately 30,000 genes. But until now, scientists did not know much about its role in the heart region. The team found that the heart and related vessels did not develop properly in mice without a normal amount of SRF.
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UNIVERSITY AMONG TOP TEN FOR TECHNOLOGY REVENUE
Companies around the world paid more than $26 million for commercial rights to the University’s research during the 2003 fiscal year, according to the latest revenue report published by the Association for University Technology Managers (AUTM). That figure, which denotes the University as the eighth highest revenue recipient in the nation, was surpassed by the latest revenue numbers that showed the University brought in more than $33 million from licensing in 2004. In addition, the report listed the University as having the fourth-highest licensing revenue in the nation for every dollar of research spending, behind only New York University, Wake Forest University, and Florida State University. The most lucrative patents include the Hib vaccine, used to prevent meningitis in children around the world, and Prevnar, which prevents several pneumococcal diseases in children.
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