| Departments — Benchmarks | Spring 2008 |
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Research Digest Absence Noted A research consortium that includes Massachusetts General Hospital has found that the deletion or duplication of a section of chromosome 16 Weed-Be-Gone When oncologists talk of stems and seeds, chances are it’s not a botanical discussion. Tumor stem cells, an immortal mutated cell type, are thought to be the seeds from which many, if not all, cancers develop. Impervious to all cancer-busting therapies, such cells are also rare, making their study difficult. Their elusiveness may now be threatened. A U.S.–China research team, with senior investigator Judy Lieberman ’81, an HMS professor of pediatrics at Children’s Hospital Boston, has produced large numbers of human breast cancer cells in mice—and has discovered a genetic switch that decreases their ability to propagate tumors. The switch, a type of molecule known as a microRNA, turned off certain genes that helped the cells spread tumors. The study appeared in the December 14, 2007, issue of Cell. What A Pain A class of drugs that is one of the more widely prescribed in developed countries may also be the source of its users’ aches and pains. A team of researchers at Beth Israel Deaconess Medical Center has found that cholesterol-lowering statins act to increase levels of atrogin-1, a protein involved in muscle atrophy. This breakdown of the muscle tissue could, says senior researcher Vikas Sukhatme ’79, the Victor J. Aresty Professor of Medicine at HMS, explain the range of symptoms, from mild muscle weakness to pain, reported by people using statins. The study appeared in the December 2007 issue of Journal of Clinical Investigation. New Cast Members Researchers have unmasked some unknown genetic players in the regulation of the blood’s levels of cholesterol and triglycerides. In the February, 2008, issue of Nature Genetics, an international team, which included scientists from the Broad Institute of Harvard and MIT, reported associating levels of these fats with 18 genetic variants, six of which had never before been linked with this activity. Lead author Sekar Kathiresan, an HMS instructor in medicine at Massachusetts General Hospital and a genetics researcher at the Broad, notes the findings may offer a way to predict a person’s risk for heart disease as well as open the door to the development of new treatments. Ann Marie Menting is associate editor of the Harvard Medical Alumni Bulletin. Photo: © iStockphoto.com/Peter Finnie |
may be a strong risk factor for autism. The researchers scanned DNA from more than 1,400 affected children and a similar number of unaffected parents and found an identical region of chromosome 16 was missing in five individuals with an autism disorder. Data from a separate group of 1,000 patients from Children’s Hospital Boston showed that among participants with a diagnosis of autism or a related developmental delay, five had the same deletion and four others had a duplication of the section. The work appeared in the February 14, 2008, issue of the New England Journal of Medicine.
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