Oncogenic senescence: a multi-functional perspective
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Darren J. Baker1,2,*, Fatouma Alimirah3,*, Jan M. van Deursen1,2, Judith Campisi3 and Jeffrey Hildesheim4
1 Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota, USA
2 Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA
3 Buck Institute for Research on Aging, Novato, California, USA
4 Division of Cancer Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
* These authors have contributed equally to this work
Darren J. Baker, email:
Fatouma Alimirah, email:
Keywords: cellular senescence, tumorigenesis, microenvironment
Received: November 11, 2016 Accepted: November 14, 2016 Published: February 25, 2017
Cellular senescence is defined as an irreversible growth arrest with the acquisition of a distinctive secretome. The growth arrest is a potent anticancer mechanism whereas the secretome facilitates wound healing, tissue repair, and development. The senescence response has also become increasingly recognized as an important contributor to aging and age-related diseases, including cancer. Although oncogenic mutations are capable of inducing a beneficial senescence response that prevents the growth of premalignant cells and promotes cancer immune-surveillance, the secretome of senescent cells also includes factors with pro-tumorigenic properties. On June 23rd and 24th, 2016, the Division of Cancer Biology of the National Cancer Institute sponsored a workshop to discuss the complex role of cellular senescence in tumorigenesis with the goal to define the major challenges and opportunities within this important field of cancer research. Additionally, it was noted how the development of novel tools and technologies are required to accelerate research into a mechanistic understanding of senescent cells in carcinogenesis in order to overcome the current limitations in this exciting, yet ill-defined area.
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