Correlation between epidermal growth factor receptor mutations and the expression of estrogen receptor-β in advanced non-small cell lung cancer

Oncol Lett. 2017 Apr;13(4):2359-2365. doi: 10.3892/ol.2017.5711. Epub 2017 Feb 10.

Abstract

Epidermal growth factor receptor (EGFR) mutations are more common in non-small cell lung cancer (NSCLC) and in female patients of East Asian origin. Therefore, the present study investigated the presence of EGFR mutations in advanced NSCLC, and assessed its correlation with clinicopathologic factors, including the expression of estrogen receptor-β (ER-β) and patient prognosis. The present study performed a retrospective analysis of 83 patients with stage IIIB-IV NSCLC. The expression of ER-β and p53 were examined using immunohistochemical methods. EGFR mutations were evaluated using the amplification refractory mutation system. The expression of ER-β and p53 were detected in 37 (45.6%) and 48 (57.8%) of the patient tumors, respectively. EGFR mutations were identified in 36 (45.4%) cases. EGFR mutations were more frequently observed in ER-β-negative tumors (26/46; 56.5%), compared with ER-β-positive tumors (10/37; 27%). The expression of ER-β was significantly associated with EGFR mutations with an odds ratio (OR) of 0.241 (P=0.029). However, no significant correlation was observed between the expression of p53 and mutations in EGFR (OR=1.792; P=0.340). In addition, the expression of ER-β and lymph node metastasis were associated with poor prognosis, whereas EGFR mutations were significantly associated with favorable prognosis in terms of progression-free survival rates. However, there was no prognostic significance associated with the expression of p53. In conclusion, the expression of ER-β was significantly correlated with the presence of EGFR mutations. The expression of ER-β and mutations of EGFR were found to be prognostic factors for survival rates in patients with advanced NSCLC.

Keywords: epidermal growth factor receptor; estrogen receptor-β; mutation; non-small cell lung cancer; p53.