Cross-talk between aging and cancer: the epigenetic language

The risk of having cancer increases with age probably because progenitor cells from mature organisms accumulate enough molecular lesions to evade the homeostatic control of their tissular contexts. Molecular lesions can be genetic (mutations, deletions, or translocations) and/or epigenetic. Epigenet...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2007-04, Vol.1100 (1), p.60-74
Main Authors: Fraga, Mario F, Agrelo, Ruben, Esteller, Manel
Format: Article
Language:English
Subjects:
Aging - genetics
Animals
Cell Proliferation
CpG Islands
Diet
DNA Methylation
Epigenesis, Genetic
Homeostasis
Humans
Models, Biological
Mutation
NAD - chemistry
Neoplasms - genetics
Neoplasms - mortality
Risk
Sirtuins - chemistry
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Summary:The risk of having cancer increases with age probably because progenitor cells from mature organisms accumulate enough molecular lesions to evade the homeostatic control of their tissular contexts. Molecular lesions can be genetic (mutations, deletions, or translocations) and/or epigenetic. Epigenetic signaling, including DNA methylation and histone modification, is essential for normal development and becomes altered during Aging and by cancer. Several epigenetic alterations, such as global hypomethylation and CpG island hypermethylation, are progressively accumulated during Aging and directly contribute to cell transformation. Intriguingly, others, such as those involved in the control of telomere length and several epigenetic enzymes belonging to the family of nicotinamide adenine dinucleotide (NAD)(+) dependent deacetylases known as sirtuins, exhibit a well-defined progression during Aging that is dramatically reverted in transformed cells. We discuss the biological significance of both groups of epigenetic modifications in terms of their relative contribution to ontogenic development, senescence, and cell proliferation.
ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1395.005