Turning anti-ageing genes against cancer

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Recent studies in diverse organisms implicate proto-oncogenic pathways, including insulin-like growth factor-I (IGF-I), Ras and AKT/protein kinase B in the ageing process. Although IGF-I is thought to contribute to cancer by promoting growth and preventing apoptosis, evidence from model organisms suggests that proto-oncogene homologues might contribute to the DNA mutations and chromosomal damage that are observed in tumour cells by increasing DNA damage, in both dividing and non-dividing cells, and involving error-prone systems in DNA repair. This raises the possibility that cancer can be reduced by chronic downregulation of pro-ageing pathways.

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Figure 1: A model for normal and oncogenic IGF-I, Ras and AKT/PKB in promoting DNA mutations.
Figure 2: IGF-I signalling, ageing and cancer.


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Related work in the laboratory of V.D.L. has been supported by an American Federation for Aging Research (AFAR) grant, by National Institutes of Health (NIH) grant AG20642 and AG025135, and by a Norris Cancer Center pilot grant. Related work has been supported by AG17242, AG20438, ES11044 and Ellison grant AG-SS-1496-05 in the laboratory of J.V. and by NIH grant CA100504 in the laboratory of M.R.L.

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Correspondence to Valter D. Longo.

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Longo, V., Lieber, M. & Vijg, J. Turning anti-ageing genes against cancer. Nat Rev Mol Cell Biol 9, 903–910 (2008) doi:10.1038/nrm2526

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