TY - JOUR
T1 - Somatic mutations, genome mosaicism, cancer and aging
AU - Vijg, Jan
N1 - Funding Information:
I would like to thank my co-workers for sharing data and insights with me, which greatly helped me writing this conceptual review. My research is supported by NIH grants AG017242, AG047200, CA180126, AG038072, the SENS Research Foundation and the The Glenn Foundation for Medical Research.
Publisher Copyright:
© 2014 .
PY - 2014/6/1
Y1 - 2014/6/1
N2 - Genomes are inherently unstable due to the need for DNA sequence variation in the germ line to fuel evolution through natural selection. In somatic tissues mutations accumulate during development and aging, generating genome mosaics. There is little information about the possible causal role of increased somatic mutation loads in late-life disease and aging, with the exception of cancer. Characterizing somatic mutations and their functional consequences in normal tissues remains a formidable challenge due to their low, individual abundance. Here, I will briefly review our current knowledge of somatic mutations in animals and humans in relation to aging, how they arise and lead to genome mosaicism, the technology to study somatic mutations and how they possibly could cause non-clonal disease.
AB - Genomes are inherently unstable due to the need for DNA sequence variation in the germ line to fuel evolution through natural selection. In somatic tissues mutations accumulate during development and aging, generating genome mosaics. There is little information about the possible causal role of increased somatic mutation loads in late-life disease and aging, with the exception of cancer. Characterizing somatic mutations and their functional consequences in normal tissues remains a formidable challenge due to their low, individual abundance. Here, I will briefly review our current knowledge of somatic mutations in animals and humans in relation to aging, how they arise and lead to genome mosaicism, the technology to study somatic mutations and how they possibly could cause non-clonal disease.
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U2 - 10.1016/j.gde.2014.04.002
DO - 10.1016/j.gde.2014.04.002
M3 - Review article
C2 - 25282114
AN - SCOPUS:84904542026
SN - 0959-437X
VL - 26
SP - 141
EP - 149
JO - Current Opinion in Genetics and Development
JF - Current Opinion in Genetics and Development
ER -
