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Archive - Mar 2, 2011

Blood Protein May Be Biomarker for Lung Cancer

Scientists have reported discovery of a protein in the blood of lung cancer patients that could possibly be used in a test for the disease — difficult to diagnose in its earliest and most treatable stages — and to develop drugs that stop lung cancer from spreading. Their study appears in the American Chemical Society’s Journal of Proteome Research. In the report, Dr. Je-Yoel Cho and colleagues in South Korea note that lung cancer is the leading cause of cancer deaths worldwide. Lung cancer is so deadly because of its tendency to metastasize to distant sites in the body, such as the liver or the brain. Early detection could improve survival rates, but it is very difficult to detect lung cancer at early stages with today's technology. To find a better diagnostic tool, the researchers studied the proteins in the blood of lung cancer patients in search of red flags that could signal the disease's presence. They focused on adenocarcinoma, which accounts for one in three cases and is the most rapidly increasing form of lung cancer in women. Dr. Cho and colleagues found elevated levels of a protein called serum amyloid A (SAA) in the blood and lung tissue of lung adenocarcinoma patients, compared to healthy people. Their work showed that high amounts of SAA were unique to lung cancers (compared with other lung diseases or other cancers) and that the protein was involved in metastasis of cancer cells from the original tumor site. The researchers said that the protein could be used as a diagnostic marker for lung cancer and as a target for developing drugs that stop metastasis. [Press release] [Journal of Proteome Research abstract]

Overlooked Enzyme May Be New Target for Lowering Cholesterol

A promising new way to potentially inhibit cholesterol production in the body has been discovered, a way that may yield treatments as effective as existing medications but with fewer side-effects. In a study published in the March 2 issue of the journal Cell Metabolism, a team of researchers from the University of New South Wales (UNSW) School of Biotechnology and Biomolecular Sciences-led by Associate Professor Andrew Brown–report that an enzyme-squalene mono-oxygenase (SM)-plays a previously unrecognized role as a key checkpoint in cholesterol production. SM is one of at least 20 enzymes involved in the assembly line when cholesterol is made throughout the body but only one of these enzymes-HMG-CoA reductase (HMGR)–is currently targeted by medications to lower cholesterol levels in the blood. "The class of drugs most commonly used to lower cholesterol-statins–are the blockbusters of the pharmaceutical world and work by inhibiting HMGR," said Professor Brown. "But HMGR is involved very early on in the assembly line, so inhibiting it affects all the other steps down the line–and other useful products it provides-and that can give rise in some people to unwanted side-effects, such as muscle pain. What's exciting about this previously overlooked SM enzyme is that it acts as a checkpoint much further down the assembly line, which should mean that it can be more specifically targeted at cholesterol production instead and leave the early part of the assembly line undisturbed. Cholesterol has developed something of a bad name, so many people don't realize that it is actually essential for a healthy body. It's needed, for example, to make sex hormones and to help build the walls of every single cell in our bodies."

10 Percent of Type 2 Diabetes Patients Have Mutation in Single Gene

A multinational study has identified four mutations in a single key gene as responsible for type 2 diabetes in nearly 10 percent of patients of white European ancestry. The study, which originated in Italy and was validated at the University of California-San Francisco (UCSF) and the University of Reims, found that defects in the HMGA1 gene led to a major drop in the body’s ability to make insulin receptors – the cell’s sensor through which insulin tells the cell to absorb sugar. This drop in insulin receptors leads to insulin resistance and type 2 diabetes, according to the paper, which was published online on March 2 in JAMA. Until now, no mutations in a single gene have been significantly associated with playing a role in type 2 diabetes. The results provide the unique opportunity for a test to predict potential for the disease in patients, as well as the possibility of identifying which of the current diabetes medications work best for people with one of the gene mutations, the authors said. Ultimately, it also could help drive research to find new and improved drugs for those patients. While the study focused on Caucasians, it also lays the groundwork for similar analyses in patients of Asian, African, and Native American descent, who suffer from higher rates of the disease, according to diabetes researcher Dr. Ira Goldfine, a UCSF professor of medicine and of physiology who led the U.S. arm of these studies. “This is a major breakthrough in type 2 diabetes,” said Dr. Goldfine, noting that 26 million Americans have diabetes and an estimated 79 million have pre-diabetes. “Many of our current diabetes drugs are very effective in some patients and not in others.