Clinicopathologic Analysis of Epidermal Growth Factor Receptor Status in Non-small Cell Lung Cancer: Protein Expression, Gene Amplification and Survival Analysis.
- Author:
Seungkoo LEE
1
;
Jene CHOI
;
Se Jin JANG
Author Information
1. Department of Pathology, Kangwon National University Hospital, Chuncheon, Korea.
- Publication Type:Original Article
- Keywords:
Carcinoma;
Non-small-cell lung;
Receptor;
Epidermal growth factor;
In situ hybridization
- MeSH:
Adenocarcinoma;
Carcinoma, Non-Small-Cell Lung*;
Carcinoma, Squamous Cell;
Epidermal Growth Factor*;
Gene Amplification;
Gene Expression*;
Genes, erbB-1;
Immunohistochemistry;
In Situ Hybridization;
In Situ Hybridization, Fluorescence;
Prognosis;
Receptor, Epidermal Growth Factor*;
Survival Analysis*;
Survival Rate
- From:Korean Journal of Pathology
2007;41(6):387-392
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Abnormal over-expression or gene amplification of epidermal growth factor receptor (EGFR) is important in the prognosis of non-small cell lung cancer (NSCLC). We investigated the frequency of EGFR protein expression and gene amplification, and the correlation between EGFR status and survival in NSCLC. METHODS: We examined 360 cases of microarrayed NSCLC tissues for the EGFR protein expression and EGFR gene amplification using immunohistochemistry and fluorescent in situ hybridization. RESULTS: EGFR protein expression and EGFR gene amplification occurred in 110 cases (30.6%) and 24 cases (6.7%), respectively. EGFR protein expression and gene amplification were more frequent in squamous cell carcinoma than in adenocarcinoma. Differences in EGFR protein expression did not dramatically affect survival curves (p=0.740), but differences in gene amplification did (p<0.05): EGFR gene amplification was associated with a lower 5-year survival rate. CONCLUSION: EGFR protein expression and gene amplification showed moderate correlation with each other. EGFR gene amplification predicted a poor prognosis, whereas EGFR protein expression did not.