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Molecular Basis of Drug Resistance: Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors and Anaplastic Lymphoma Kinase Inhibitors / 결핵및호흡기질환
Tuberculosis and Respiratory Diseases ; : 188-198, 2013.
Article in English | WPRIM | ID: wpr-157868
ABSTRACT
Over the past decade, several kinase inhibitors have been approved based on their clinical benefit in cancer patients. Unfortunately, in many cases, patients develop resistance to these agents via secondary mutations and alternative mechanisms. To date, several major mechanisms of acquired resistance, such as secondary mutation of the epidermal growth factor receptor (EGFR) gene, amplification of the MET gene and overexpression of hepatocyte growth factor, have been reported. This review describes the recent findings on the mechanisms of primary and acquired resistance to EGFR tyrosine kinase inhibitors and acquired resistance to anaplastic lymphoma kinase inhibitors, primarily focusing on non-small cell lung carcinoma.
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Full text: Available Index: WPRIM (Western Pacific) Main subject: Phosphotransferases / Protein-Tyrosine Kinases / Drug Resistance / Hepatocyte Growth Factor / Receptor Protein-Tyrosine Kinases / Protein Kinase Inhibitors / Epidermal Growth Factor / ErbB Receptors / Lung / Lymphoma Limits: Humans Language: English Journal: Tuberculosis and Respiratory Diseases Year: 2013 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Phosphotransferases / Protein-Tyrosine Kinases / Drug Resistance / Hepatocyte Growth Factor / Receptor Protein-Tyrosine Kinases / Protein Kinase Inhibitors / Epidermal Growth Factor / ErbB Receptors / Lung / Lymphoma Limits: Humans Language: English Journal: Tuberculosis and Respiratory Diseases Year: 2013 Type: Article