title: KRAS mutations predict response to EGFR inhibitors.
abstract: Five antiepidermal growth factor receptor therapies have been approved for the treatment of solid tumors. However, response rates are relatively low. Several biomarkers that enrich for patients with tumors most likely to respond to these therapeutic agents have been identified. Mutations in the intermediate signal transduction pathway member KRAS also selects patients with tumors depending on signaling through this pathway. However, because KRAS acts downstream of the EGF receptor, somatic changes in this gene can be used as a marker to exclude patients unlikely to benefit from anti-EGFR therapy. Recent clinical data have provided substantial evidence that KRAS mutational status should be utilized as a diagnostic marker for predicting that response to anti-EGFR therapies in colorectal and non-small cell lung cancer.
authors.affiliation: Centocor R&D, 145 King of Prussia Road, Radnor, PA 19086, USA. mraponi1@cntus.jnj.com
authors.forename: Mitch
authors.initials: M
authors.lastname: Raponi
authors.forename: Hans
authors.initials: H
authors.lastname: Winkler
authors.forename: Nicholas C
authors.initials: NC
authors.lastname: Dracopoli
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D018450:Disease Progression; D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D005787:Gene Frequency; D006801:Humans; D009154:Mutation; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D013534:Survival; D018631:ras Proteins / Q000235:genetics*
chemical_list: D000970:Antineoplastic Agents; C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins