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Short-term gain, long-term pain: the senescence life cycle and cancer

期刊

GENES & DEVELOPMENT
卷 33, 期 3-4, 页码 127-143

出版社

COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.320937.118

关键词

senescence; cancer; epigenetics; inflammation

资金

  1. University of Cambridge
  2. Cancer Research UK
  3. Hutchison Whampoa
  4. Cancer Research UK Cambridge Institute core grant [C14303/A17197]
  5. Cancer Research UK Early Detection Pump Priming award [C20/A20976]
  6. Medical Research Council [MR/R010013/1]
  7. Tokyo Tech World Research Hub Initiative
  8. MRC [MR/R010013/1] Funding Source: UKRI

向作者/读者索取更多资源

Originally thought of as a stress response end point, the view of cellular senescence has since evolved into one encompassing a wide range of physiological and pathological functions, including both protumorignic and antitumorigenic features. It has also become evident that senescence is a highly dynamic and heterogenous process. Efforts to reconcile the beneficial and detrimental features of senescence suggest that physiological functions require the transient presence of senescent cells in the tissue microenvironment. Here, we propose the concept of a physiological senescence life cycle, which has pathological consequences if not executed in its entirety.

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