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Nature 454, 172-173 (10 July 2008) | doi:10.1038/454172a; Published online 9 July 2008
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Postdoctoral Position, Endocrine Unit
- MGH-Harvard Medical School
- MGH, 50 Blossom Street, Boston MA 02114
Executive Director
- Pennington Biomedical Research Center
- Baton Rouge, Louisiana, USA
Cancer: An unexpected addiction
John D. Shaughnessy1
Abstract
Both oncogenes and normal genes can mediate the development and progress of cancer. What used to separate their effects was cancer's dependence on, or 'addiction' to, oncogenes but not normal genes. Not any more.
A central tenet of cancer is that it arises from a single cell through progressive acquisition of genetic mutations that lead to the activation of oncogenes (cancer-promoting genes) and/or inactivation of tumour-suppressor genes. Cancer's 'addiction' to oncogenes is sometimes so strong that even brief inactivation of a single oncogene can cause remission in model systems1, 2, implying that oncogenes are the 'Achilles' heel' of cancers3.
- John D. Shaughnessy is at the Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Email: shaughnessyjohn@uams.edu
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