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REVIEW
Year : 2018  |  Volume : 4  |  Issue : 3  |  Page : 70-74

Senescence and Cancer


1 Department of Microbiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing, China; Department of Radiation Oncology, Weill Medical College of Cornell University, New York, NY, USA
2 Department of Radiation Oncology, Weill Medical College of Cornell University, New York, NY, USA
3 Department of Microbiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing, China

Correspondence Address:
Prof. Li Liu
Department of Microbiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing 100005
China
Wen H Shen
Department of Radiation Oncology, Weill Medical College of Cornell University, New York, NY 10065
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ctm.ctm_22_18

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Senescence is a double-edged sword that can function in opposite directions. It is a potential mechanism for a cell to avoid malignant transformation. However, senescence can also promote cancer development by altering the cellular microenvironment through a senescence-associated secretory phenotype (SASP). At least, three types of cellular stress such as activation of oncogenes, loss of tumor suppressor genes, and chemo/radiotherapy can induce cell senescence. Oncogene-induced senescence can be intertwingly associated with the replicative senescence. Early-stage senescence may protect cell from transformation, while prolonged senescence often promotes cancer development. This review will focus on the characteristics of senescence, discuss the regulation of senescence during cancer development, and highlight the complexity of senescence that makes cancer treatment challenging.


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