Activated signaling through the small guanosine triphosphatase Ras is often associated with abnormal proliferation of cancer cells. Stites et al. used a combination of mathematical modeling and experiments to gain new insights into the regulatory properties of the network of factors that influence Ras (or are regulated by it) and how these factors are altered in cancer cells. Their results offer insight into why particular activating Ras mutants, but not others, are found in cancer cells, and suggest a pharmacological strategy that may preferentially impede excessive signaling in networks containing an oncogenically mutated form of Ras while sparing normal cells.
- Unraveling Ras Interactions
A model of cell signaling reveals why only one mutated form of an oncogene occurs in tumors and suggests a strategy for selective inhibition of oncogene-containing cells.Permalink: