Cancer risk increases with age, and scientists have long perceived a possible evolutionary tradeoff between longer lifespan and greater risk of cancer. Now, researchers at Fox Chase Cancer Center find direct evidence for that tradeoff in new data showing that expression of a key tumor suppressor protein induces premature aging in mice. Although scientists know that loss of p16 is associated with numerous human tumors, they know much less about the function of p16 in normal cells and tissues. To explore this, Greg H. Enders, from Fox Chase Cancer Center (Pennsylvania, USA), and colleagues engineered a strain of mice that enables them to control p16 expression in various tissues and at various times in an animal's lifespan. They quickly found that turning on p16 blocked cell proliferation in normal tissues. The implications of blocked cell proliferation emerged when they expressed p16 in animals that were not yet fully mature. "They developed features of premature aging," Enders reported. "To my knowledge, this is the first model that induces striking characteristics of premature aging where there is no macromolecular damage. The premature aging appears to be the result of blocking cell proliferation."