Journal
MOLECULAR & CELLULAR ONCOLOGY
Volume 3, Issue 5, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/23723556.2016.1190885
Keywords
Cancerogenesis; DNA single-strand breaks; keratincytes; oxidative stress; p16; p38MAPK; senescence; XRCC1
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Funding
- Center National de la Recherche Scientifique
- Universite Lille 1
- Universite Lille 2
- Ligue contre le Cancer
- Association pour la Recherche sur le Cancer
- Institut Pasteur de Lille
- SIRIC OncoLille [INCa-DGOS-Inserm 6041]
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In contrast to fibroblasts, epithelial cells spontaneously escape from senescence and develop clones of mutated, transformed, and tumorigenic cells. Recently, we revealed that accumulation of unrepaired DNA single-strand breaks is a trigger of the p16 (CDKN2)-dependent cell cycle arrest pathway in senescent epithelial cells and also the mutagenic motor of post-senescence neoplastic escape.
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