Somatic cell mutations: Can they provide a link between aging and cancer?

Mitchell S. Turker

Research output: Contribution to journalArticlepeer-review

32 Scopus citations

Abstract

Cancers increase during aging in mammals, and an accumulating body of evidence suggests that mutational events too do likewise. Mutational events are intimately involved in the malignant process. One current view is that mutator phenotypes are required in malignant cells for a sufficient number of critical target genes to be affected. These mutator phenotypes are believed to result from underlying deficiencies in genes necessary to maintain genomic stability. This review will provide a framework for a discussion of cancer and aging by detailing with a pair of wise approach studies that address the relations between aging, cancer, and mutations. Results from these studies will be used to suggest that a mutator phenotype develops in the cells of older individuals in the absence of an underlying genetic deficiency. Instead, it is proposed that a mixture of chromosomal aberrations, DNA damage, and chronic exposure to genotoxic forces, including oxidative stress, provide the basis for this age-accelerated mutator phenotype. (C) 2000 Elsevier Science Ireland Ltd.

Original languageEnglish (US)
Pages (from-to)1-19
Number of pages19
JournalMechanisms of Ageing and Development
Volume117
Issue number1-3
DOIs
StatePublished - Aug 15 2000

Keywords

  • Aging
  • Cancer
  • Genomic instability
  • Mutator phenotype
  • Oxidative stress

ASJC Scopus subject areas

  • Aging
  • Developmental Biology

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