Chemoprevention meets glucose control.

The report by Memmott et al. (beginning on page 1066 in this issue of the journal) assessing the efficacy of the antidiabetes drug metformin in a mouse model of lung carcinogenesis suggests protective effects via two possible avenues: Decreased circulating insulin and insulin-like growth factor levels and energy stress leading to inhibition of mammalian target of rapamycin signaling. These potential mechanisms are discussed in this perspective, as are their implications for cancer prevention and therapy.