Aging and cancer cell biology, 2009

被引:68
作者
Campisi, Judith [1 ,2 ]
Yaswen, Paul [2 ]
机构
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA
关键词
DNA damage response; FOXO transcription factors; inflammation; longevity; p53; PI3; kinases; sirtuins; telomeres; tumor suppression; GENOME MAINTENANCE; DEACETYLASE SIRT1; MICE; SENESCENCE; TELOMERES; TUMORIGENESIS; GROWTH; DAMAGE; LONGEVITY;
D O I
10.1111/j.1474-9726.2009.00475.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cancer is an age-related disease in organisms with renewable tissues. A malignant tumor arises in part from genomic damage, which can also drive age-related degeneration. However, cancer differs from many age-related degenerative diseases in that it entails gain-of-function changes that confer new (albeit aberrant) properties on cells, resulting in vigorous cell proliferation and survival. Nonetheless, interventions that delay age-related degeneration - for example, caloric restriction or dampened insulin/IGF-1 signaling - often also delay cancer. How then is the development of cancer linked to aging? The answer to this question is complex, as suggested by recent findings. This Hot Topic review discusses some of these findings, including how genomic damage might alter cellular properties without conferring mutations, and how some genes that regulate lifespan in organisms that lack renewable tissues might affect the development of cancer in mammals.
引用
收藏
页码:221 / 225
页数:5
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