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ONCOLOGY: Genetic Deletion Hikes Protein, Causes Cancer Last March, the British journal Lancet reported the apparently miraculous recovery of four patients with a rare blood disorder. The patients, who were suffering from hypereosinophilic syndrome (HES), were brought back from the brink of death by taking low doses of the much-touted drug Gleevec (imatinib). Now, Gary Gilliland, Elizabeth Stover, Jan Cools (l to r), and their colleagues report that they have confirmed the stunning results in nine more HES patients. They also have found out how and why the drug works, a discovery that has taken them right to the heart of what causes the deadly disease in the first place. Their findings, reported in the March 27 New England Journal of Medicine, could provide a new model for how some cancers arise.
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PUBLIC HEALTH: Forecasting Method Predicts Floods of Drug-resistant Bacteria Multidrug-resistant strains of Streptococcus pneumoniae may rise at a shockingly fast rate in the next two years. The grim forecast comes from a mathematical model explaining the jumps and dips in antimicrobial resistance from state to state, reported in the April 2003 Nature Medicine (online March 10) by Marc Lipsitch (on left), Alethea McCormick, and colleagues. Further calculations suggest that local antibiotic use is to blame.
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DEVELOPMENTAL BIOLOGY: Red Cells Use Transporter Protein for Cell Division A team led by Leonard Zon (left) and Barry Paw discovered a new role for a common red blood cell protein, band 3. Paw initially was intrigued by a zebrafish mutant with an unusual quality: about a third of its red blood cells had two nuclei, as if they had failed to divide. In tracking down the cause of the condition, the team was surprised to find that band 3, a protein specific to red blood cells and some kidney cells, was the culprit. In a paper online March 31 in Nature Genetics, the team shows that red blood cells have incorporated band 3 into cell division--an unusual case of a cell-specific adaptation for a universal process.
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Copyright 2003 by the President and Fellows of Harvard College
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