Characteristics of the included studies

A total of 476 articles were screened from the databases, and 17 eligible articles including 1,458 patients were selected (Figure 1 and Table 1).15–31 The publication dates ranged from 1998 to 2015, sample size from 18 to 199, and maximum follow-up time from 25 to 180 months. On NOS scoring, five articles were rated 6 points, one article was rated 7 points, and only one article was rated 8 points. Among all the included studies, only two were prospective studies, and the rest were retrospective studies. In most studies, specimens were fixed with formalin and embedded with paraffin. The treatment of tumor tissues was not clearly defined in two studies. IHC was performed in all studies. Of the 17 articles, seven reported the available HR and 10 provided the Kaplan–Meier curves. Considering glioma subgroups, 10 studies focused on GBM, two studies focused on ependymoma, two focused on low-grade glioma (LGG), one focused on astrocytoma, one included anaplastic astrocytoma (AA) and GBM, and one included glioma of various subgroups and grades. No study reported disease-free survival or PFS.

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(To view a larger version of Table 1, click here.)

Prognostic significance of EGFR expression in glioma patients

A total of 1,458 glioma patients were included in the survival analysis. The pooled HR was 1.72 (95% CI 1.32–2.25, P=0.000, random effect; Figure 2). High expression of EGFR had a significant relationship with poor prognosis for glioma patients.

(To view a larger version of Figure 2, click here.)

Due to the emergence of high heterogeneity in the study (I2=79.8%, Ph=0.000), a subgroup analysis was conducted to further explore the source of heterogeneity. The subgroups included tumor types, publication years, region, study design, sample size, cutoff value, maximum follow-up time, source of HR, and quality score (Table 2). High EGFR expression was significantly associated with reduced OS in GBM (HR 1.57, 95% CI 1.15–2.14, P=0.004) and mixed gliomas (HR 1.95, 95% CI 1.37–2.77, P=0.000), but not in LGG (HR 1.67, 95% CI 0.037–7.62, P=0.508). There was substantial heterogeneity in GBM (I2=83.8%, Ph=0.000), while heterogeneity was not found in LGG (I2=0%, Ph=0.731) and mixed gliomas (I2=0%, Ph=0.522). In subgroups of publication years, study design, sample size, source of HR, and quality score, the following predicted poor survival: publication year <2010 (HR 1.95, 95% CI 1.37–2.77, P=0.000); publication year ≥2010 (HR 1.52, 95% CI 1.10–2.10, P=0.011); retrospective study (HR 1.75, 95% CI 1.39–2.19, P=0.000); sample size <100 (HR 1.99, 95% CI 1.54–2.57, P=0.000); sample size ≥100 (HR 1.43, 95% CI 1.04–2.97, P=0.027); HRs extracted from the Kaplan–Meier curves (HR 2.10, 95% CI 1.71–2.58, P=0.000); quality score <7 (HR 1.37, 95% CI 1.00–1.87, P=0.048); and quality score ≥7 (HR 1.72, 95% CI 1.32–2.25, P=0.000).

(To view a larger version of Table 2, click here.)

Apparent heterogeneity existed in the subgroup of publication year ≥2010 (I2=80.2%, Ph=0.000), prospective study (I2=81.1%, Ph=0.000), sample size ≥100 (I2=85.5%, Ph=0.000), HRs that were reported (I2=69.5%, Ph=0.003), and quality score ≥7 (I2=84.8%, Ph=0.000). Low heterogeneity existed in the subgroup of publication year <2010 (I2=45.6%, Ph=0.065) and retrospective study (I2=45.8%, Ph=0.024). Sample size <100 (I2=0%, Ph=0.501) and quality score <7 (I2=0%, Ph=0.618) did not show heterogeneity.