GENETICS: Toxic to Tasty
As a rule, antibiotics kill bacteria. Or so we used to think. According to a study in the April 4 Science, hundreds of different strains of bacteria found in the soil cannot only survive an antibiotic assault, they thrive on it. More than 600 types of bacteria, many of which are close relations to those that infect humans, were able to grow on a diet of nothing but antibiotic drugs. The antibiotics tested included 18 clinically relevant drugs. The paper, by co–first authors Morten Sommer (left) and Gautam Dantas (right) from the lab of George Church, suggest that the extent of the “antibiotic resistome,” the collection of genetic mechanisms that enable resistance, is much broader than expected.

STRATEGIC PLANNING: Advisory Group Shares Vision for Technology Infrastructure
The Tools and Technology advisory group within Dean Jeffrey Flier’s strategic planning process has issued preliminary recommendations. They include boosting investment in the technologies of therapeutics, imaging, and computation; upgrading core facilities; creating an Initiative on Technology Innovation; and lowering barriers to technology sharing. Heading the group are Stephen Harrison (left) and Elazer Edelman (right).

CARDIOLOGY: Mutations in Adults Illuminate Heart Defect in Children
Flaws in the blueprint for the heart’s exquisite tapestry of sarcomere proteins cause most cases of hypertrophic cardiomyopathy in adults. A team led Christine and Jonathan Seidman has now determined that many children with unexplained cardiac hypertrophy harbor mutations in the same genes. Their study, which appeared online April 9 in The New England Journal of Medicine, provides the first evidence that unexplained cardiac hypertrophy can share common genetic roots, regardless of the age at which symptoms appear.

ONCOLOGY: Cancer Drug Takes Fast Track to Clinical Trials
Gary Gilliland (left) and his team, including primary researcher Gerlinde Wernig, report the striking efficacy of a new designer drug in treating a mouse model of the red blood cell cancer, polycythemia vera (PV). More than 95 percent of patients with PV have been previously found to express a mutant version of the kinase protein JAK2. In the April 7 Cancer Cell, Gilliland’s team shows that a specially designed small-molecule inhibitor of JAK2 can revert a mouse model of PV into remission—apparently without any significant side effects. This new drug is now undergoing phase I clinical trials at the Dana–Farber Cancer Institute.

Copyright 2008 by the President and Fellows of Harvard College