Molecular damage in cancer: an argument for mTOR-driven aging

被引：70

作者：

Blagosklonny, Mikhail V. ^{[1
]}

机构：

[1] Roswell Pk Canc Inst, Dept Cell Stress Biol, Buffalo, NY 14263 USA

来源：

AGING-US | 2011年 / 3卷 / 12期

关键词：

cancer; target; therapy; leukemia; anticancer drugs; NF-KAPPA-B; ONCOGENE-INDUCED SENESCENCE; CELL-CYCLE ARREST; TRANSMISSIBLE VENEREAL TUMOR; CALORIE RESTRICTION MIMETICS; TERM DIETARY RESTRICTION; HEMATOPOIETIC STEM-CELLS; LIFE-SPAN EXTENSION; DNA-DAMAGE; GENOMIC INSTABILITY;

D O I：

10.18632/aging.100422

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Despite common belief, accumulation of molecular damage does not play a key role in aging. Still, cancer (an age-related disease) is initiated by molecular damage. Cancer and aging share a lot in common including the activation of the TOR pathway. But the role of molecular damage distinguishes cancer and aging. Furthermore, an analysis of the role of both damage and aging in cancer argues against "a decline, caused by accumulation of molecular damage" as a cause of aging. I also discuss how random molecular damage, via rounds of multiplication and selection, brings about non-random hallmarks of cancer.

引用

页码：1130 / 1141

页数：12

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