Format

Send to

Choose Destination
Trends Cancer. 2016 Oct;2(10):552-560. doi: 10.1016/j.trecan.2016.09.004.

The evolution of lifespan and age-dependent cancer risk.

Author information

1
Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, CO 80045.
2
Integrated Department of Immunology, University of Colorado School of Medicine, Aurora, CO 80045.
3
Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO 80045.
4
Department of Medicine, Section of Hematology, University of Colorado School of Medicine, Aurora, CO 80045.

Abstract

The Armitage-Doll multi-stage model of carcinogenesis tremendously refocused cancer science by postulating that carcinogenesis is driven by a sequence of genetic changes in cells. Age-dependent cancer incidence thus has been explained in terms of the time necessary for oncogenic mutations to occur. While the multi-step nature of cancer evolution is well-supported by evidence, the mutation-centric theory is unable to explain a number of phenomena, such as the disproportion between cancer frequency and animal body size or the scaling of cancer incidence to animal lifespan. In this paper, we present a theoretical review of the current paradigm and discuss some fundamental evolutionary theory postulates that explain why cancer incidence is a function of lifespan and physiological, not chronological, aging.

PMID:
28439564
PMCID:
PMC5400291
DOI:
10.1016/j.trecan.2016.09.004
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center