Fig. 8From: Pharmacological targeting of the ephrin receptor kinase signalling by GLPG1790 in vitro and in vivo reverts oncophenotype, induces myogenic differentiation and radiosensitizes embryonal rhabdomyosarcoma cellsEffects of GLPG1790 combined or not with irradiation on in vivo tumour growth. a Growth curve of tumour volumes from xenografted TE671 cell lines, untreated (vehicle), GLPG1790-treated (GLPG1790), irradiated (RT), GLPG1790-pretreated and irradiated (RT + GLPG1790). Tumour volumes were evaluated as describes in methods and represent the mean ± SEM of 10 mice. The upper panel shows the sequential treatments of xenografted mice started when tumours reached a volume of approximate 0.5 cm3. GLPG1790 (30 mg/kg) was administered 5 days a week for 2 weeks and before each irradiation, administered on alternate days. b Tumour weights in mice untreated or treated with GLPG1790, radiotherapy or combined treatment. c Kaplan-Meier estimates for rates of progression for untreated (vehicle), GLPG1790, RT, or GLPG1790 + RT combination in TE671-derived tumours. d Phosphorylation/activation status of EPH-A2, EPH-B, ERKs, AKTs and levels of Ki-67 protein in tumours from vehicle, RT, GLPG1790, or GLPG1790 + RT-treated mice (a, b). Representative Western blot experiment of the 10 tumours analysed. Total EPH-A2, EPH-B, ERKs, AKTs and α-Tubulin immunoblotting were used as loading control (lower panel)Back to article page