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
在 En
| WPRIM
| ID: wpr-157868
Responsible library:
WPRO
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.
Key words
全文:
1
索引:
WPRIM
主要主题:
Phosphotransferases
/
Protein-Tyrosine Kinases
/
Drug Resistance
/
Hepatocyte Growth Factor
/
Receptor Protein-Tyrosine Kinases
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Protein Kinase Inhibitors
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Epidermal Growth Factor
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ErbB Receptors
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Lung
/
Lymphoma
限制:
Humans
语言:
En
期刊:
Tuberculosis and Respiratory Diseases
年:
2013
类型:
Article