scholarly journals TRANSFORMATION TO SMALL CELL LUNG CANCER AFTER PLATINUM‐BASED DOUBLET THERAPY IN PATIENTS OF LUNG ADENOCARCINOMA WITH WILD TYPE EPIDERMAL GROWTH FACTOR RECEPTOR: A CASE REPORT

Respirology ◽  
2019 ◽  
Vol 24 (S2) ◽  
pp. 183-184
Keyword(s):  
Lung Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Case Report ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Small Cell ◽  
Wild Type ◽  
Small Cell Lung ◽  
Epidermal Growth

scholarly journals Evaluation of erlotinib for the treatment of patients with non-small cell lung cancer with epidermal growth factor receptor wild type

2017 ◽  
Vol 14 (1) ◽  
pp. 306-312 ◽  
Author(s):  
Fumihiko Hirai ◽  
Makoto Edagawa ◽  
Shinichiro Shimamatsu ◽  
Ryo Toyozawa ◽  
Gouji Toyokawa ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Small Cell Lung Cancer ◽  
Growth Factor Receptor ◽  
Small Cell ◽  
Wild Type ◽  
Small Cell Lung ◽  
Epidermal Growth

scholarly journals Erlotinib in wild type epidermal growth factor receptor non-small cell lung cancer: A systematic review

2013 ◽  
Vol 8 (4) ◽  
pp. 204 ◽  
Author(s):  
Abdul-Rahman Jazieh ◽  
Reem Al Sudairy ◽  
Nada Abu-Shraie ◽  
Wafaa Al Suwairi ◽  
Mazen Ferwana ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Systematic Review ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Small Cell ◽  
Wild Type ◽  
Small Cell Lung ◽  
Epidermal Growth

Role of Epidermal Growth Factor Receptor Inhibitors in Epidermal Growth Factor Receptor Wild-Type Non–Small-Cell Lung Cancer

2013 ◽  
Vol 31 (8) ◽  
pp. 1061-1069 ◽  
Author(s):  
Scott A. Laurie ◽  
Glenwood D. Goss
Keyword(s):  
Lung Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Small Cell Lung Cancer ◽  
Growth Factor Receptor ◽  
Small Cell ◽  
Wild Type ◽  
Small Cell Lung ◽  
Epidermal Growth

Worldwide, the majority of patients with advanced non–small-cell lung cancer (NSCLC) do not have activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR). These wild-type patients comprise a significant proportion of those treated with inhibitors of this pathway, and data from randomized trials suggest that some of these wild-type patients will derive a modest benefit from these agents. Although the detection of an activating mutation predicts for a greater likelihood of response and longer progression-free survival from an EGFR tyrosine kinase inhibitor, currently there are no biomarkers that consistently and reproducibly predict for lack of benefit in wild-type patients. Several strategies to increase the efficacy of these inhibitors in wild-type NSCLC are the subject of ongoing investigations.

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