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Somatic mutations, genome mosaicism, cancer and aging
被引:96
|作者:
Vijg, Jan
[1
]
机构:
[1] Albert Einstein Coll Med, Dept Genet, New York, NY 10461 USA
关键词:
COPY-NUMBER-VARIATION;
DETECTABLE CLONAL MOSAICISM;
DE-NOVO MUTATIONS;
L1;
RETROTRANSPOSITION;
CHROMOSOMAL MOSAICISM;
CHILDHOOD-CANCER;
HUMAN BRAIN;
DNA-DAMAGE;
AGE;
DISEASE;
D O I:
10.1016/j.gde.2014.04.002
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
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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页码:141 / 149
页数:9
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