home   genetic news   bioinformatics   biotechnology   literature   journals   ethics   positions   events   sitemap
 
  HUM-MOLGEN -> Genetic News | search  
 

Cancer Suppression Puts Cells Under Arrest

 
  August, 10 2005 4:16
your information resource in human molecular genetics
 
     
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

print this article mail this article
Bookmark and Share this page (what is this?)

Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.

Use the links below to share this article on the social bookmarking site of your choice.

Read more about social bookmarking at Wikipedia - Social Bookmarking

Latest News
Variants Associated with Pediatric Allergic Disorder

Mutations in PHF6 Found in T-Cell Leukemia

Genetic Risk Variant for Urinary Bladder Cancer

Antibody Has Therapeutic Effect on Mice with ALS

Regulating P53 Activity in Cancer Cells

Anti-RNA Therapy Counters Breast Cancer Spread

Mitochondrial DNA Diversity

The Power of RNA Sequencing

‘Pro-Ageing' Therapy for Cancer?

Niche Genetics Influence Leukaemia

Molecular Biology: Clinical Promise for RNA Interference

Chemoprevention Cocktail for Colon Cancer

more news ...

Generated by News Editor 2.0 by Kai Garlipp
WWW: Kai Garlipp, Frank S. Zollmann.
7.0 © 1995-2017 HUM-MOLGEN. All rights reserved. Liability, Copyright and Imprint.