Interconnection between Senescence and Cancer

Dear Colleagues,

Cellular senescence occurs in response to various stressors, including DNA damage, oxidative stress and oncogene activation. Senescence acts primarily as a tumour suppression mechanism that prevents proliferation of potentially cancerous cells. Senescence cells secrete plethora of factors, including inflammatory cytokines, growth factors, and proteases, collectively known as the senescence-asscociated secretory phenotype (SASP). SASP can stimulate immunosurveillance mechanisms and potent the tumor suppresive function of senescent cells. On the other hand, the accumulation of senescent cells in vivo exerts detrimental effects on the functionality of tissues and organs. Chronic accumulation of senescent cells also promote tumor relapse and metastasis. Thus, the Jekyll and Hyde nature of cellular senescence is highly complex, and understanding the regulatory mechanisms of cellular senescence will lead to the development of therapies for various diseases, including cancer, neurodegenerative diseases and diabetes. This Special Issue provides an open access forum aimed at compiling a collection of original research and review articles on the interconnection between senescence and cancer.

Dr. Yasumichi Inoue
Dr. Chi-Ming Wong
Dr. Andy T. Y. Lau
Guest Editors

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