BRAFE600-associated senescence-like cell cycle arrest of human naevi

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 () and Daniel S. Peeper ()
Additional contact information
Chrysiis Michaloglou: Division of Molecular Genetics
Liesbeth C. W. Vredeveld: Division of Molecular Genetics
Maria S. Soengas: University of Michigan
Christophe Denoyelle: University of Michigan
Thomas Kuilman: Division of Molecular Genetics
Chantal M. A. M. van der Horst: Academic Medical Centre
Donné M. Majoor: The Netherlands Cancer Institute
Jerry W. Shay: The University of Texas Southwestern Medical Center
Wolter J. Mooi: Free University Medical Centre
Daniel S. Peeper: Division of Molecular Genetics

Nature, 2005, vol. 436, issue 7051, 720-724

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
References: Add references at CitEc
Citations: View citations in EconPapers (5)

Downloads: (external link)
https://www.nature.com/articles/nature03890 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:436:y:2005:i:7051:d:10.1038_nature03890

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature03890

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().