GeneAlert ... from UPI

LEPROSY GENOME TRACES MIGRATIONS

The leprosy genome tells the story of human migrations, French researchers report in the journal Science. A genetics study comparing strains of leprosy-causing bacteria has revealed the world's existing leprosy infections are all caused by a single bacterial clone that has spread yet barely mutated for centuries. The study also shows the disease may have begun in East Africa, as opposed to India as previously thought, and then spread to the other continents in part through European colonialism and later via the slave trade. The new findings indicate the disease actually originated in East Africa or perhaps the Near East, then migrated eastward and westward. The ability to trace an infection back to a certain region may help public health workers monitor the movement of the disease over time and determine the geographic source of new infections, according to study author Stewart Cole of the Pasteur Institute in Paris.

CANCER PROTEIN STRUCTURE FOUND

California scientists at the Scripps Research Institute have solved the structure of a protein involved in resisting antibiotics and chemotherapy. The structure of this membrane transporter protein -- MsbA -- is described in the current issue of the journal Science. Bacteria use these transporters to nullify antibiotics, and human cancer cells have similar membrane transporters on their surfaces that undermine the potency of chemotherapy drugs. "We actually have very good drugs to fight cancer and to kill bacteria," says Geoffrey Chang. "(But) they can't always get in the cells to work." The structures Chang and Christopher Reyes solved using high-resolution X-ray crystallography reveal molecular details that could be useful for improving cancer therapy and fighting antibiotic-resistant bacteria.

SCIENTISTS INHIBIT MUTANT GENE LINKED TO TUMORS

By studying mice with skin cancer, researchers at the Huntsman Cancer Institute at the University of Utah found a way to inhibit a mutant gene. The mutant gene is found in up to 30 percent of human tumors. The gene Ras -- when normal -- is important in cell signaling, or communication among cells. When mutated, however, Ras is an "oncogene" or cancer-causing gene that has been shown to promote the growth of cancers in the pancreas, colon and lung, as well as thyroid cancer and leukemia. The researchers explain in the journal Proceedings of the National Academy of Sciences they have discovered an enzyme that, when inhibited, appears to reduce the incidence of Ras-induced tumors in mice.

SCIENTISTS HONORED FOR GENE TARGETING

Two U.S. scientists have jointly received the March of Dimes Prize in Developmental Biology for developing an indispensable tool for genetic disease research. Drs. Oliver Smithies, of the University of North Carolina at Chapel Hill School of Medicine, and Mario R. Capecchi, of the University of Utah, are being honored for developing gene targeting. Their technique gives scientists around the world the ability to alter particular genes in cultured cells and transfer those targeted genes to laboratory mice. Gene targeting thus allows researchers to design and produce "knockout" lab mice to study how the disabled gene works. Because humans share the vast majority of their genes with mice, gene-targeted mice are used to reproduce diseases that occur in humans.

MOUSE GENE ACCOUNTS FOR BLOOD ABNORMALITIES

Mice that develop a Parkinson's-like deterioration when deprived of a gene for iron metabolism were also linked to developing anemia, a U.S. study found. Researchers at the National Institute of Child Health and Human Development of the National Institutes of Health learned the mice have high blood levels of a compound known as protoporphyrin IX. This compound is converted into heme, the compound that allows red blood cells to carry oxygen to the tissues. The mice also have microcytic anemia-abnormally small red blood cells. The researchers also found the mice developed anemia and blood abnormalities sometimes seen in people with a rare condition known as erythropoietic protoporphyria. "This study provides additional clues that may contribute to our understanding of neurodegenerative disorders that appear to involve iron metabolism," says Dr. Duane Alexander, director of the NICHD. The study was published in the journal Blood.

DRUG MAY INHIBIT PROTEIN LINKED TO HEART ATTACK

Researchers and deCODE Genetics Inc., Reykjavik, Iceland, think they have a drug that inhibits a specific protein that increases the risk of heart attack. The researchers found that levels of several of the biomarkers linked to arterial inflammation and risk of myocardial infarction, or MI, decreased in response to DG-031 with the production of leukotriene B4 significantly reduced. "When taken together, the data from our MI gene-isolation study and the clinical trial reported herein show that DG-031 is a safe and well-tolerated drug that affects a biochemical defect that confers a relative risk of acute cardiovascular events, which is similar to or greater than that conferred by the top quartile of LDL cholesterol," according to the researchers. The researchers found that levels of several of the biomarkers linked to arterial inflammation and risk of MI decreased in response to DG-031 with the production of leukotriene B4 significantly reduced.

--

(EDITORS: For more information on LEPROSY contact Jessica Lawrence-Hurt at 202-326-7088 or jlawrenc@aaas.org. For PROTEIN, Jason Bardi at 858-784-9254 or jasonb@scripps.edu. For TUMORS, Linda Aagard at 801-587-7639 or linda.aagard@hci.utah.edu. For GENE TARGETING, Michele Kling at 914-997-4613. For MOUSE GENE, Robert Bock or 301-496-5133.