A new study has found that altering food schedules and light/dark exposure in mice modified the expression of circadian clock genes and genes involved in carcinogenesis and tumor progression. The circadian clock regulates the approximate 24-hour cycles of many animals, including mammals. It has been reported that tumors grow faster in animals with a disrupted circadian clock--which happens, for example, in chronic jet lag--but the molecular mechanism is unclear. Francis Lévi, M.D., Ph.D., of the French National Institute of Health and Medical Research (INSERM) and University Paris XI at Paul Brousse Hospital in Villejuif, France, and colleagues compared the expression patterns of circadian clock and cell cycle genes in the livers and tumors of mice synchronized by normal light and dark schedules (normal circadian clock) or with schedules designed to simulate chronic jet lag in humans (disrupted circadian clock). They found that meal timing reversed the disrupted circadian clock gene expression patterns and slowed tumor growth in chronic jet lagged mice. The authors conclude that the altered light/dark or feeding schedules modified the expression of circadian clock genes and genes involved in carcinogenesis and tumor progression.