RTI uses cookies to offer you the best experience online. By clicking “accept” on this website, you opt in and you agree to the use of cookies. If you would like to know more about how RTI uses cookies and how to manage them please view our Privacy Policy here. You can “opt out” or change your mind by visiting: http://optout.aboutads.info/. Click “accept” to agree.
Hayes, T., Stratford, J., Wang-Gillam, A., & Der, C. J. (2014). Ras genes and cancer. In A. Wittinghofer (Ed.), Ras superfamily small G proteins: Biology and mechanisms 1 (Vol. 1, pp. 157-171). Springer.
The three RAS genes (HRAS, KRAS, and NRAS) comprise the most commonly mutated oncogene family in human cancer. RAS genes encode highly related small GTPases that are key regulators of cytoplasmic signaling networks that include the Raf-MEK-ERK mitogen-activated protein kinase cascade and the PI3K-Akt signaling cascade. There is increasing evidence that all RAS mutations are “not created equal” and that mutation specific therapies may be needed, that there will not be a “one size fits all” anti-Ras therapy. In this chapter, we summarize the frequency and nature of RAS mutations in human cancers, with a focus on the two cancers with the highest frequency of RAS mutations, pancreatic ductal adenocarcinoma (95 %), and colorectal (40 %) cancers.