Journal
CANCER RESEARCH
Volume 69, Issue 20, Pages 7917-7925Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-08-2510
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Funding
- PPF Bioinformatique of Lille 1 University [F16R-CT2003-508842]
- Association pour la Recherche contre le Cancer
- Ligue contre le Cancer
- Caused Regional NPdC
- European Regional Development Fund
- RISC-RAD [F16R-CT2003-508842]
- Institut Pasteur de Lille, Region NPdC, and Societe Francaise du Cancer
- Ministry of Research and FRM
- [EDF V3-103]
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Studies on human fibroblasts have led to viewing senescence as a barrier against tumorigenesis. Using keratinocytes, we show here that partially transformed and tumorigenic cells systematically and spontaneously emerge from senescent cultures. We show that these emerging cells are generated from senescent cells, which are still competent for replication, by an unusual budding-mitosis mechanism. We further present data implicating reactive oxygen species that accumulate during senescence as a potential mutagenic motor of this post-senescence emergence. We conclude that senescence and its associated oxidative stress could be a tumor-promoting state for epithelial cells, potentially explaining why the incidence of carcinogenesis dramatically increases with advanced age. [Cancer Res 2009;69(20):7917-25]
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