Abstract

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.

Author affiliations

1. Valter D. Longo and Michael R. Lieber are at the Andrus Gerontology Center, the Molecular and Computational Biology Department and the Norris Cancer Center, University of Southern California, 3715 McClintock Avenue, Los Angeles, California 90089–0191, USA.
2. Jan Vijg is at the Albert Einstein College of Medicine, Department of Genetics, 1301 Morris Park Avenue, Bronx, New York 10461, USA.

Correspondence to: Valter D. Longo¹ Email: vlongo@usc.edu

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