Abstract
PurposeTo investigate whether FGFR1 gene amplification is associated with clinicopathologic characteristics and its potential impact on survival in patients with resected esophageal squamous cell carcinoma (ESCC).MethodsFive hundred fifty-six ESCC patients undergoing curative resection of ESCC were retrospectively studied. FGFR1 gene copy number was determined in microarrayed tumor samples using fluorescent in situ hybridization (FISH) analysis. FGFR1 gene amplification status was prespecified as copy number ≥ 6 or FGFR1/CEN 8 ratio ≥ 2.2. FGFR1 expression was evaluated by immunohistochemistry. Overall survival (OS) and disease-free survival (DFS) were analyzed using the Kaplan-Meier method followed by the log rank test. Correlation with survival was examined using multivariate Cox regression.ResultsFGFR1 amplification was identified in 67 (12.1%) patients; these patients had significantly shorter OS (50.0 vs 32.0 months; log rank; P<0.001) as well as shorter DFS (47.0 vs 28.0 months; log rank; P<0.001) than those without FGFR1 amplification. Under a Cox proportional hazard model, FGFR1 amplification was associated with significantly shorter OS (adjusted hazard ratio [AHR]=1.61; 95% CI, 1.10-2.43, P=0.004) and DFS (AHR=1.72; 95%CI, 1.15-2.48; P<0.001). Moreover, cases with high intratumoral FGFR1 expression showed significantly shorter OS and DFS than those with low FGFR1 expression. The frequency of FGFR1 amplification was significantly higher in heavy drinkers than in moderate and light drinkers.ConclusionFGFR1 amplification is an independent adverse prognostic factor in surgically resected ESCC. FGFR1 may be a promising therapeutic target in patients with ESCC.
Highlights
Esophageal cancer is one of the most aggressive malignancies [1, 2]
Under a Cox proportional hazard model, Fibroblast growth factor receptor 1 (FGFR1) amplification was associated with significantly shorter Overall survival (OS) and disease-free survival (DFS) (AHR=1.72; 95% confidence interval (95%CI), 1.15-2.48; P
Loga et al investigated the prevalence of FGFR1 amplification in a tissue microarray containing 346 esophageal adenocarcinomas and 254 esophageal squamous cell carcinoma (ESCC) using dual-labeling fluorescent in situ hybridization (FISH) analysis and found that FGFR1 amplification correlated with the histologic subtype of ESCC (9.4% vs. esophageal adenocarcinoma 1.6%, P
Summary
Esophageal cancer is one of the most aggressive malignancies [1, 2]. Esophageal squamous cell carcinoma (ESCC), the predominant histological type in east Asia, is considered as an environmental malignancy attributable to tobacco smoking and alcohol intake [3]. Loga et al investigated the prevalence of FGFR1 amplification in a tissue microarray containing 346 esophageal adenocarcinomas and 254 ESCCs using dual-labeling fluorescent in situ hybridization (FISH) analysis and found that FGFR1 amplification correlated with the histologic subtype of ESCC (9.4% vs esophageal adenocarcinoma 1.6%, P
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