K-ras as a target for lung cancer therapy

J Thorac Oncol. 2008 Jun;3(6 Suppl 2):S160-3. doi: 10.1097/JTO.0b013e318174dbf9.


K-ras is currently accepted to be the most frequently mutated oncogene in non-small cell lung cancer. In addition, tumors harboring mutant K-ras seem to be refractory to most available systemic therapies, making K-ras an attractive target for cancer therapy. The complexity of K-ras signaling presents many opportunities for therapeutic targeting. A number of different approaches aimed at abrogating K-ras activity have been explored in clinical trials. Several of the putative K-ras-directed therapeutic agents tested have demonstrated clinical activity. However, many of these agents have multiple targets, and their antitumor effects may not be due to K-ras inhibition. To date, no selective, specific inhibitor of the K-ras pathway is available for routine clinical use.

Publication types

  • Review

MeSH terms

  • Benzamides / administration & dosage
  • Benzenesulfonates / administration & dosage
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / mortality
  • Clinical Trials, Phase I as Topic
  • Clinical Trials, Phase II as Topic
  • Drug Delivery Systems
  • Drugs, Investigational / administration & dosage*
  • ErbB Receptors / antagonists & inhibitors*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, ras / drug effects*
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics
  • Lung Neoplasms / mortality
  • Male
  • Niacinamide / analogs & derivatives
  • Phenylurea Compounds
  • Prognosis
  • Pyridines / administration & dosage
  • Risk Factors
  • Sensitivity and Specificity
  • Sorafenib
  • Survival Analysis
  • Treatment Outcome


  • 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide
  • Benzamides
  • Benzenesulfonates
  • Drugs, Investigational
  • Phenylurea Compounds
  • Pyridines
  • Niacinamide
  • Sorafenib
  • ErbB Receptors