Abstract
BackgroundThis study was designed to investigate EGFR protein expression, EGFR copy number and EGFR mutations in lung adenocarcinomas, to explore the relationship of the three markers.MethodsEGFR status was analyzed in surgically resected lung adenocarcinoma samples from 133 Chinese patients by three methods: protein expression (n = 133) by standardized immunohistochemistry (IHC), gene copy number (n = 133) by fluorescence in situ hybridization (FISH), and mutation analysis using the Scorpion amplification refractory mutation system (ARMS) (n = 133).ResultsThe results showed that 68.4% of the samples were positive by IHC, 42.1% were positive by FISH, and 63.9% contained activating kinase domain mutations. EGFR mutations were more frequent in non-smoking patients (p = 0.008), and EGFR mutations were associated with EGFR FISH positivity (p < 0.0001). When using 10% positivity and 2+ as cutoffs, EGFR protein expression was significantly correlated with EGFR FISH positivity (p = 0.012) and EGFR mutations (p = 0.008) after Bonferroni correction.ConclusionEGFR protein expression, EGFR copy number and EGFR mutations were closely related to each other. Standard methods and interpretation criteria need to be established.
Highlights
This study was designed to investigate EGFR protein expression, EGFR copy number and EGFR mutations in lung adenocarcinomas, to explore the relationship of the three markers
After Bonferroni correction for 5 comparisons, P < 0.01 were considered significant, EGFR mutations were significantly associated with smoking status, and were not associated with age, gender, lymph node metastasis or tumor stage (p ≥ 0.01) (Table 1)
We found that 42.1% (56/133) of lung adenocarcinomas showed EGFR fluorescence in situ hybridization (FISH) positivity, and that EGFR FISH positivity was more frequent in late stages than in early stages of lung adenocarcinomas
Summary
This study was designed to investigate EGFR protein expression, EGFR copy number and EGFR mutations in lung adenocarcinomas, to explore the relationship of the three markers. EGFR-targeted therapy has proven effective in treating non-small cell lung cancer (NSCLC). The agents approved for the treatment of NSCLC are monoclonal antibodies (MoAbs) directed against EGFR and small-molecule TK inhibitors (TKIs). Increased EGFR gene copy number as detected by FISH was strongly correlated with response, progressionfree survival (PFS) and overall survival (OS) after treatment with EGFR TK inhibitors (TKI) in previous studies. These results suggested that a high EGFR gene copy number is a strong indicator of TKI sensitivity [7,8]
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