Fig 1: Growth hormone receptor (GHR) overexpression is linked with functional STAT5 signalling in vitro, increased circulating hGH in patients and increased suppressor of cytokine signalling 2 (SOCS2) promoter methylation. (A) GHR and epidermal growth factor receptor (EGFR) expression levels in a series of 19 glioblastoma (GBM) patient-derived cell lines (PDCLs) as determined by RT-qPCR. Y-axis represents 2-? CT for each gene relative to PPIA expression. The threshold of 2-? CT = .2 (80th percentile value for both genes) is represented by the grey line. (B) Expression data of GHR, EGFR and SOCS2 of samples shown in panel A were averaged for GHRlow and GHRhigh subgroups. (C) Western blot showing p-STAT5 in PDCLs exposed to 221-ng/ml growth hormone (GH) (10 nM) with or without 349-ng/ml AZD1480 JAK2 inhibitor (1 µM). Densitometric values were normalized to actin levels. (D) Concentration of GH (pg/ml) detected in supernatants of GBM PDCLs after 45 h of culture. **p = .01; *p = .05 compared to culture medium. (E) Plasmatic GH concentration in patients with GBMGHR high or GBMGHR low (n = 28). (F) SOCS2 expression level in PDCLs from GHRlow and GHRhigh groups exposed (+) or not (-) to 221 ng/ml (10 nM) GH for 24 h. HEK293 cells stably overexpressing GHR (HEK293 GHR wild type [WT]) were used as positive control. (G) SOCS2 promoter methylation in a panel of PDCLs (n = 9) or GBMs tumours (n = 20), grouped as GHRlow or GHRhigh. ****p = .0001 as calculated by ANOVA two-way test