Access
To read this story in full you will need to login or make a payment (see right).
News and Views
Nature 454, 172-173 (10 July 2008) | doi:10.1038/454172a; Published online 9 July 2008
Open Innovation Challenges
-
Methods of Modeling Adaptation in Populations
The analysis of adaptation with a population is a frequently encountered computational modeling scen...
-
Optimizing Sub-cellular Localization Tags
The Seeker is looking for methods to optimize sub-cellular localization tags for protein expression....
nature jobs
Manager (Department : Patents)
- Piramal HealthCare
- Mumbai 400080 India
Manager Client Services
- Indegene Lifesystems Pvt. Ltd
- Bengaluru 560 071 India
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
To read this story in full you will need to login or make a payment (see right).
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
RESEARCH
Preclinical activity of P276-00, a novel small-molecule cyclin-dependent kinase inhibitor in the therapy of multiple myelomaLeukemia Original Article
IRF4 addiction in multiple myelomaNature Letters to Editor (10 Jul 2008)
Mesenchymal stem cells from multiple myeloma patients display distinct genomic profile as compared with those from normal donorsLeukemia Original Article

