IN TUMORIGENESIS, c-ras gene alterations occur in the form of constitutively activating point mutations that uncouple the signal transduction pathway from external stimuli, resulting in a constant proliferative signal. Normal c-ras is activated by pathways consisting of growth factors, growth factor receptors, adapter molecules, and guanine nucleotide-releasing factors. Activated c-ras then recruits raf-1 to the plasma membrane resulting in its activation and initiation of the mitogen- activated protein (MAP) kinase cascade. Concurrent with the identification of pathway molecules, investigators have identified a number of methods to inhibit the effects of c-ras in tumor cells, including the rap1A tumor suppressor gene and dominant negative rasN17. Further identification of intracellular signaling molecules and methods to manipulate these pathways will be essential in the quest to develop effective anticancer agents.
|Original language||English (US)|
|Number of pages||12|
|State||Published - Jan 1 1995|
ASJC Scopus subject areas
- Cancer Research