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. 2018 Jul 9;14(7):e1007175. doi: 10.1371/journal.ppat.1007175

Fig 6. Multi tyrosine kinase inhibitors that can target PDGFRA block KSHV-mediated tumorigenesis.

Fig 6

(A) Tumor growth curve from mice with established subcutaneous mECK36 tumors treated with vehicle (PBS) or Imatinib (150 mg/Kg twice daily) by oral administration. Data indicate mean tumor size ± SD (n = 10). (B) mRNA levels of VEGFA in Imatinib treated and control mECK36 tumors determined by RT-qPCR. (C) Tumor growth curve from mice with established subcutaneous mECK36 tumors treated with vehicle (PBS) or Sunitinib (80 mg/Kg/day) by oral administration. Data indicate mean tumor size ± SD (n = 10). (D) Phosphorylated and total PDGFR levels from Imatinib-treated, Sunitinib-treated and control mECK36 tumors determined by immunoblotting. (E) IFA of frozen sections of Imatinib-treated, Sunitinib-treated and control tumors stained with pan-endothelial marker CD31 (red) or lymphatic microvessel marker VEGFR3 (red). Nuclei were counterstained with DAPI (blue). Bar graphs show the relative intensity signals of CD31 and VEGFR3 from 10 different fields. *P < 0.05.