Senescence in premalignant tumours

Manuel Collado, Jesús Gil, Alejo Efeyan, Carmen Guerra, Alberto J. Schuhmacher, Marta Barradas, Alberto Benguría, Angel Zaballos, Juana M. Flores, Mariano Barbacid, David Beach and Manuel Serrano ()
Additional contact information
Manuel Collado: Spanish National Cancer Centre (CNIO)
Jesús Gil: MRC Clinical Sciences Centre, Imperial College, Hammersmith
Alejo Efeyan: Spanish National Cancer Centre (CNIO)
Carmen Guerra: Spanish National Cancer Centre (CNIO)
Alberto J. Schuhmacher: Spanish National Cancer Centre (CNIO)
Marta Barradas: Spanish National Cancer Centre (CNIO)
Alberto Benguría: Spanish National Centre of Biotechnology (CNB-CSIC)
Angel Zaballos: Spanish National Centre of Biotechnology (CNB-CSIC)
Juana M. Flores: Complutense University
Mariano Barbacid: Spanish National Cancer Centre (CNIO)
David Beach: Centre for Cutaneous Research, Institute of Cell and Molecular Science
Manuel Serrano: Spanish National Cancer Centre (CNIO)

Nature, 2005, vol. 436, issue 7051, 642-642

Abstract: Cell senescence and cancer Cellular senescence, a growth-arrest program that limits the lifespan of mammalian cells and prevents unlimited cell proliferation, is attracting considerable interest because of its links to tumour suppression. Using a mouse model in which the oncogene Ras is activated in the haematopoietic compartment of bone marrow, Braig et al. show that cellular senescence can block lymphoma development. Genetic inactivation of the histone methyltransferase Suv39h1 that controls senescence by ‘epigenetic’ modification of DNA-associated proteins, or a pharmacological approach that mimics loss of this enzyme, allow the formation of malignant lymphomas in response to oncogenic Ras. This work has important implications for both tumour development and tumour therapy. Michaloglou et al. report that oncogene-induced senescence may be a physiologically important process in humans, keeping moles in a benign state for many years: unchecked they develop into malignant melanomas. Chen et al. also find that cellular senescence blocks tumorigenesis in vivo: they show that acting together, the p53 tumour suppressor and the cellular senescence system can prevent prostate cancer induction in mice by the PTEN mutation. Collado et al. show that cellular senescence is a defining feature of Ras-initiated premalignant tumours; this could prove valuable in the diagnosis and prognosis of cancer. See the web focus .

Date: 2005
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DOI: 10.1038/436642a

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