BRAFE600-associated senescence-like cell cycle arrest of human naevi View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2005-08

AUTHORS

Chrysiis Michaloglou, Liesbeth C. W. Vredeveld, Maria S. Soengas, Christophe Denoyelle, Thomas Kuilman, Chantal M. A. M. van der Horst, Donné M. Majoor, Jerry W. Shay, Wolter J. Mooi, Daniel S. Peeper

ABSTRACT

Cell senescence and cancerCellular 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. More... »

PAGES

720-724

Journal

TITLE

Nature

ISSUE

7051

VOLUME

436

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature03890

DOI

http://dx.doi.org/10.1038/nature03890

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16079850


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