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The age of cancer

Abstract

A striking link exists between advanced age and increased incidence of cancer. Here I review how several of the age-related molecular and physiological changes might act in concert to promote cancer, and in particular epithelial carcinogenesis. Experimental data indicate that the aged, cancer-prone phenotype might represent the combined pathogenetic effects of mutation load, epigenetic regulation, telomere dysfunction and altered stromal milieu. Further verification of the role of these effects should in turn lead to the design of effective therapeutics for the treatment and prevention of cancer in the aged.

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Figure 1: Cancer incidence as a function of age.
Figure 2: Tumour spectrum in human and mouse.
Figure 3: Fusion–bridge–breakage mechanism and cytogenetic profiles.
Figure 4: Dysfunctional telomere-induced genomic instability model of epithelial carcinogenesis.

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Acknowledgements

I apologize to my colleagues whose relevant work I was unable to cite owing to space and reference limitations. I thank J. Vijg, D. Hanahan, J. Campisi, J.-P. Issa, N. Schreiber-Agus, G. Merlino, S. Mellis, L. Chin, S. Weiler and members of my laboratory for helpful discussions and critical comments. R.A.D. is supported by the National Institutes of Health and is an American Cancer Society Research Professor and a Steven and Michele Kirsch Foundation Investigator.

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Correspondence to Ronald A. DePinho.

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DePinho, R. The age of cancer. Nature 408, 248–254 (2000). https://doi.org/10.1038/35041694

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