Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication

Raffaella Di Micco, Marzia Fumagalli, Angelo Cicalese, Sara Piccinin, Patrizia Gasparini, Chiara Luise, Catherine Schurra, Massimiliano Garre’, Paolo Giovanni Nuciforo, Aaron Bensimon, Roberta Maestro, Pier Giuseppe Pelicci and Fabrizio d’Adda di Fagagna ()
Additional contact information
Raffaella Di Micco: IFOM Foundation – FIRC Institute of Molecular Oncology Foundation
Marzia Fumagalli: IFOM Foundation – FIRC Institute of Molecular Oncology Foundation
Angelo Cicalese: European Institute of Oncology
Sara Piccinin: Experimental Oncology 1, Centro di Riferimento Oncologico CRO IRCCS
Patrizia Gasparini: IFOM Foundation – FIRC Institute of Molecular Oncology Foundation
Chiara Luise: IFOM Foundation – FIRC Institute of Molecular Oncology Foundation
Catherine Schurra: Genome Stability Unit, 75724 Pasteur Institute
Massimiliano Garre’: IFOM Foundation – FIRC Institute of Molecular Oncology Foundation
Paolo Giovanni Nuciforo: IFOM Foundation – FIRC Institute of Molecular Oncology Foundation
Aaron Bensimon: Genomic Vision
Roberta Maestro: Experimental Oncology 1, Centro di Riferimento Oncologico CRO IRCCS
Pier Giuseppe Pelicci: European Institute of Oncology
Fabrizio d’Adda di Fagagna: IFOM Foundation – FIRC Institute of Molecular Oncology Foundation

Nature, 2006, vol. 444, issue 7119, 638-642

Abstract: Cancer and cell senescence Cancer is commonly thought of as uncontrolled cellular proliferation, but in the early stages of many cancers, oncogene expression is associated with cellular senescence. A possible explanation for this has now been found. Two groups report a link between oncogene-induced senescence and the DNA damage response. Activated oncogenes can cause aberrant DNA replication and thereby DNA damage that can lead to cell senescence. Cellular senescence was found previously to be a barrier to tumorigenesis in vivo, so oncogene-induced senescence may be an innate defence against cancer. But its effectiveness is often disabled by further mutations. Understanding the relationship between cell senescence and tumour formation may aid in the development of diagnostic and prognostic tools based on senescence markers.

Date: 2006
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DOI: 10.1038/nature05327

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