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Archive - Apr 11, 2011

New Mechanism of Tumor Invasiveness Discovered

Researchers at the Hebrew University of Jerusalem have discovered a previously unknown mechanism whereby tumor cells invade normal tissues, spreading cancer through various organs. The ability of tumor cells to invade adjacent structures is a prerequisite for metastasis and distinguishes malignant tumors from benign ones. Thus, understanding the mechanisms that drive malignant cells to invade and a possible avenue for halting that mechanism could have tremendous potential for enhancing early detection of malignant cells and for therapeutic treatment.It has previously been assumed that tumor cells turn invasive upon accumulation of multiple mutations, each giving the cancer cell some invasive properties. Now, Professor Yinon Ben-Neriah and Dr. Eli Pikarsky of the Institute for Medical Research Israel-Canada at the Hebrew University Faculty of Medicine and their colleagues are reporting an alternative mechanism through which tumor cells become invasive. They found a program that is operated by a concerted group of genes that, when activated together, confer invasive properties upon epithelial cells. (Epithelial tissues line the cavities and surfaces of structures throughout the body, and also form many glands.) An article reporting their work appeared in the February 17, 2011 issue of the journal Nature. Interestingly, the expression of this entire gene group is normally suppressed by a single gene – p53 – that is considered as the most important tumor suppressor but unfortunately is inactivated in the majority of human cancers. Some key properties of the protein produced by the p53 gene -- arresting cell growth and induction of cell death – were previously discovered by Dr. Moshe Oren of the Weizmann Institute of Science, another member of the current research team.

Saturated Fatty Acids and Type 2 Diabetes

A diet high in saturated fat is a key contributor to type 2 diabetes, a major health threat worldwide. Several decades ago scientists noticed that people with type 2 diabetes have overly active immune responses, leaving their bodies rife with inflammatory chemicals. In addition, people who acquire the disease are typically obese and are resistant to insulin, the hormone that removes sugar from the blood and stores it as energy. For years no one has known exactly how the three characteristics are related. But a handful of studies suggest that they are inextricably linked. New research from the University of North Carolina at Chapel Hill School of Medicine adds clarity to the connection. The study published online April 10, 2011, in the journal Nature Immunology finds that saturated fatty acids, but not the unsaturated type can activate immune cells to produce an inflammatory protein, called interleukin-1beta.“The cellular path that mediates fatty acid metabolism is also the one that causes interleukin-1beta production,” says senior study co-author Dr. Jenny Y. Ting, William Kenan Rand Professor in the Department of Microbiology and Immunology. “Interleukin-1beta then acts on tissues and organs such as the liver, muscle and fat (adipose) to turn off their response to insulin, making them insulin-resistant. As a result, activation of this pathway by fatty acid can lead to insulin resistance and type 2 diabetes symptoms.” Dr. Ting is also a member of the UNC Lineberger Comprehensive Cancer Center, and the UNC Inflammatory Diseases Institute. [Press release] [Nature Immunology abstract]

Cold and Asthma Virus Grown in Tissue Culture

Using sinus tissue removed during surgery at University of Wisconsin Hospital and Clinics, researchers at the University of Wisconsin-Madison have managed to grow a recently discovered species of human rhinovirus (HRV), the most frequent cause of the common cold, in culture. The researchers found that the virus, which is associated with up to half of all HRV infections in children, has reproductive properties that differ from those of other members of the HRV family. The accomplishments, reported in Nature Medicine on April 10, 2011, should allow antiviral compounds to be screened to see if they stop the virus from growing. The report sheds light on HRV-C, a new member of the HRV family that also includes the well-known HRV-A and HRV-B. Discovered five years ago, HRV-C has been notoriously difficult to grow in standard cell cultures and, therefore, impossible to study. "We now have evidence that there may be new approaches to treating or preventing HRV-C infections," says senior author Dr. James Gern, professor of medicine at the UW-Madison School of Medicine and Public Health and an asthma expert at American Family Children's Hospital. Future drugs could be especially useful for children and adults who have asthma and other lung problems, Dr. Gern says. Recent studies have shown that in addition to its major role in the common cold, HRV-C is responsible for between 50 percent and 80 percent of asthma attacks. HRV-C is a frequent cause of wheezing illnesses in infants and may be especially likely to cause asthma attacks in children. HRV infections of all kinds also can greatly worsen chronic lung diseases such as cystic fibrosis and chronic obstructive pulmonary disease. Like other scientists, Dr. Yury Bochkov, a virologist in Gern's lab, was unable to grow HRV-C in standard cell lines.