An intriguing study in the September 24 Journal of Biology—published by BioMed Central, a sister company of The Scientist—suggests there could be a previously unrecognized anticancer benefit from treatment with some common antidiabetic drugs. Simon A. Hawley and colleagues at the University of Dundee show how the tumor suppressor protein kinase LKB1 is linked to AMP-activated protein kinase (AMPK), the target enzyme for several drugs commonly used to treat type 2 diabetes (Journal of Biology, 2:28, September 24, 2003).

AMPK acts as a "metabolic master switch," reducing glucose levels and inhibiting biosynthetic pathways and cell proliferation. A lack of, or a mutation in, the LKB1 gene gives rise to Peutz-Jeghers syndrome, an autosomal dominant human disorder in which the risk of developing malignant tumors in some tissues is 15-fold higher than normal. Both the activation pattern of AMPK and the LKB1 substrate have been...

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