Joan Brugge and colleagues have uncovered a mechanism by which the body kills potential tumor cells. When cells separate from their normal environment—a common event during tumor formation—they develop certain metabolic disabilities that prevent them from becoming cancerous. While some tumor genes can help the cells correct such defects, the researchers also found that antioxidant treatment could restore metabolic activity in these homeless cells, giving them a second chance to survive and potentially become cancerous. The study appeared online Aug. 19 in Nature.

In mid-August, Focus spoke with David Rosenthal, director of Harvard University Health Services, for an update on Harvard’s H1N1 flu preparedness strategies, lessons learned, and contingency plans for decision-making in a context of urgency, uncertainty, and limited information.

By combining lab research and rugged clinical work in resource-poor countries, Anne Goldfeld is trying to make a dent in the global co-epidemic of HIV and tuberculosis. Some doubly infected patients respond well to treatment, while others die even with the best of care. Goldfeld has found that the origin of the TB involved could play a role. According to her study in the July 1 PLoS ONE, different strains of TB are more or less potent at driving HIV growth in immune cells, because they vary in their ability to stimulate the production of immune proteins that boost HIV replication. The study shows how complex interactions between the two pathogens and the immune system determine the outcome of infection.