|
Cellular senescence - a growth-arrest programme thought to end the allotted lifespan of mammalian cells and thereby prevent unlimited cell proliferation - is attracting considerable interest because of its links to tumour suppression. Four studies appearing in the 04 August 2005 issue of Nature (Vol. 436, No. 7051, pp 660-665, 725-730, 720-724 & 642) show that senescence does indeed get induced in vivo to put the break on cancer-causing genes.
Researchers led by Clemens Schmitt use a mouse model in which the cancer gene Ras is activated in the blood-forming cells of bone marrow; the team shows that cellular senescence is capable of blocking lymphoma development. Their work has important implications not only for understanding tumour development but also for treatment. Pier Paolo Pandolfi and colleagues describe how senescence, acting with the tumour suppressor p53, can prevent the development of prostate cancer in mice. Another team, led by Daniel Peeper, found that cell cycle arrest keeps moles in a benign state for years, and without it they could develop into malignant melanomas. Finally, in a Brief Communication, Manuel Serrano and colleagues also demonstrate this cell growth arrest in pre-malignant tumours, and identify new markers associated with cellular senescence. "The work identifies much-needed markers of senescence, and further delineates the molecular underpinnings of this key tumour-suppressing process," write Norman Sharpless and Ronald DePinho in a related News and Views article. CONTACT Clemens A. Schmitt
Max-Delbrück-Center for Molecular Medicine, Berlin, Germany
E-mail: clemens.schmitt@charite.de Pier Paolo Pandolfi
Memorial Sloan-Kettering Cancer Center, New York, NY, USA
E-mail: p-pandolfi@ski.mskcc.org Daniel S. Peeper
The Netherlands Cancer Institute, Amsterdam, The Netherlands
E-mail: d.peeper@nki.nl Manuel Serrano
Spanish National Cancer Centre, Madrid, Spain
E-mail: mserrano@cnio.es Ronald DePinho
Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
E-mail: ron_depinho@dfci.harvard.edu (C) Nature press release.
Message posted by: Trevor M. D'Souza
|