表观遗传学
癌症
端粒
基因组不稳定性
癌变
背景(考古学)
生物
衰老
成功老龄化
疾病
炎症
长寿
细胞衰老
生物信息学
癌症研究
医学
免疫学
遗传学
老年学
内科学
DNA损伤
表型
基因
古生物学
DNA
作者
Carlos López-Otı́n,Federico Pietrocola,David Roiz‐Valle,Lorenzo Galluzzi,Guido Kroemer
标识
DOI:10.1016/j.cmet.2022.11.001
摘要
SummaryBoth aging and cancer are characterized by a series of partially overlapping "hallmarks" that we subject here to a meta-analysis. Several hallmarks of aging (i.e., genomic instability, epigenetic alterations, chronic inflammation, and dysbiosis) are very similar to specific cancer hallmarks and hence constitute common "meta-hallmarks," while other features of aging (i.e., telomere attrition and stem cell exhaustion) act likely to suppress oncogenesis and hence can be viewed as preponderantly "antagonistic hallmarks." Disabled macroautophagy and cellular senescence are two hallmarks of aging that exert context-dependent oncosuppressive and pro-tumorigenic effects. Similarly, the equivalence or antagonism between aging-associated deregulated nutrient-sensing and cancer-relevant alterations of cellular metabolism is complex. The agonistic and antagonistic relationship between the processes that drive aging and cancer has bearings for the age-related increase and oldest age-related decrease of cancer morbidity and mortality, as well as for the therapeutic management of malignant disease in the elderly.
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