Abstract
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.
MeSH terms
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Benzamides / administration & dosage
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Benzenesulfonates / administration & dosage
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Carcinoma, Non-Small-Cell Lung / drug therapy*
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Carcinoma, Non-Small-Cell Lung / genetics
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Carcinoma, Non-Small-Cell Lung / mortality
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Clinical Trials, Phase I as Topic
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Clinical Trials, Phase II as Topic
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Drug Delivery Systems
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Drugs, Investigational / administration & dosage*
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ErbB Receptors / antagonists & inhibitors*
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Female
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Gene Expression Regulation, Neoplastic
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Genes, ras / drug effects*
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Humans
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / genetics
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Lung Neoplasms / mortality
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Male
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Niacinamide / analogs & derivatives
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Phenylurea Compounds
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Prognosis
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Pyridines / administration & dosage
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Risk Factors
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Sensitivity and Specificity
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Sorafenib
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Survival Analysis
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Treatment Outcome
Substances
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2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide
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Benzamides
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Benzenesulfonates
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Drugs, Investigational
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Phenylurea Compounds
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Pyridines
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Niacinamide
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Sorafenib
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ErbB Receptors