Syndicate content

Archive - Nov 6, 2013

Research Reveals Possible Cause of Diabetic Cardiomyopathy

Researchers from the University of Texas Medical Branch (UTMB) at Galveston have discovered one of the pathogenic components of diabetes in the heart, as published onine on October 22, 2013 in the Journal of Biological Chemistry. While both heart disease and diabetes are widely studied, how diabetic cardiomyopathy develops is not well understood, other than that it seemed to be linked to protein kinase C (PKC) — a family of enzymes that controls the functions of other proteins by using phosphates to turn them on and off. Researchers at UTMB, led by assistant professor of biochemistry Dr. Muge Kuyumcu-Martinez, studied the effects of PKC signals in the hearts of diabetic mice. "We now know that the leading cause of diabetic cardiomyopathy can be attributed to PKC activation and its downstream effects on gene expression," said Dr. Kuyumcu-Martinez. "Knowing how cardiomyopathy manifests, further research can use these results to concentrate on the prevention and treatment of heart failure in diabetics." Cardiomyopathy, a known symptom of diabetes, occurs when the muscles of the heart weaken, and the heart is no longer strong enough to pump blood and properly circulate it throughout the body. Adults with diabetes are two to four times more likely to die of heart failure than the rest of the population. The researchers discovered that when PKC is over-activated, the cells of the adult heart revert to splicing methods used during the embryonic stages. Genes contain codes for certain processes and products, such as proteins, and they send signals to the body to complete these processes and products through messenger RNA. Alternative splicing occurs when one gene contains the codes for multiple proteins.

Genetic Aberration in TOP2A Paves the Way for New, Potentially Rapidly Implemented Treatment for Some Colorectal Cancer Patients

Researchers from the Faculty of Health and Medical Sciences, University of Copenhagen, have characterized a genetic aberration in a group of colorectal cancer patients. The discovery gives hope for a new and efficient treatment of colorectal cancer, which is a frequent and often fatal disease. The research was recently published online on October 21, 2013 in the Scandinavian Journal of Gastroenterology. Approximately 600,000 patients die of colorectal cancer each year worldwide. 12-15 years of development and millions of dollars are typically the costs, when companies develop a new anti-cancer drug. Therefore all short-cuts to a treatment are welcome. Researchers at Department of Veterinary Disease Biology, University of Copenhagen, recently discovered such a potential short-cut. “Our new research shows that we might be able to introduce a treatment faster and cheaper than usual in the development of cancer treatment, and we estimate that it will be efficient in around 10 per cent of patients with colorectal cancer," says M.D. and Ph.D. student Sune Nygård, Department of Veterinary Disease Biology, University of Copenhagen. In the new study, the researchers have shown that approximately 10 per cent of colorectal cancer patients harbor an aberration in the gene called TOP2A (DNA topoisomerase 2-) in their cancer cells. These tumors could potentially benefit from treatment with a specific chemotherapeutic drug, a so-called “anti-TOP2A treatment,” which is already used in breast cancer patients with this gene aberration. “If the first treatment doesn’t cure a patient with colorectal cancer, the possibilities of additional treatment are limited,” says Nils Brünner, M.D., professor at the University of Copenhagen. “Therefore it is very important to find a new, efficient treatment,” he adds.