Somatic Mutations in the Tyrosine Kinase Domain of Epidermal Growth Factor Receptor (EGFR) Abrogate EGFR-Mediated Radioprotection in Non–Small Cell Lung Carcinoma

2007 ◽  
Vol 67 (11) ◽  
pp. 5267-5274 ◽  
Author(s):  
Amit K. Das ◽  
Benjamin P. Chen ◽  
Michael D. Story ◽  
Mitsuo Sato ◽  
John D. Minna ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Somatic Mutations ◽  
Small Cell Lung Carcinoma ◽  
Growth Factor Receptor ◽  
Kinase Domain ◽  
Small Cell ◽  
Tyrosine Kinase Domain ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Epidermal Growth

scholarly journals Development of epidermal growth factor receptor tyrosine kinase inhibitors against EGFR T790M. Mutation in non small-cell lung carcinoma

Open Medicine ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. 68-77 ◽  
Author(s):  
Yuli Wang ◽  
Zhitao Guo ◽  
Yang Li ◽  
Qinghua Zhou
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Small Cell Lung Carcinoma ◽  
Acquired Resistance ◽  
Growth Factor Receptor ◽  
Small Cell ◽  
Small Cell Lung ◽  
T790m Mutation ◽  
Cell Lung Carcinoma ◽  
Epidermal Growth ◽  
Egfr T790m

AbstractIndividualized therapies targeting epidermal growth factor receptor (EGFR) mutations show promises for the treatment of non small-cell lung carcinoma (NSCLC). However, disease progression almost invariably occurs 1 year after tyrosine kinase inhibitor (TKI) treatment. The most prominent mechanism of acquired resistance involves the secondary EGFR mutation, namely EGFR T790M, which accounts for 50%–60% of resistant tumors. A large amount of studies have focused on the development of effective strategies to treat TKI-resistant EGFR T790M mutation in lung tumors. Novel generations of EGFR inhibitors are producing encouraging results in patients with acquired resistance against EGFR T790M mutation. This review will summarize the novel inhibitors, which might overcome resistance against EGFR T790M mutation.

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