Notably, immunoblot analysis of these cells showed that compared to normal ECs, GBM-associated ECs, isolated from either intratumor or peri-tumor tissue, exhibited diminished expression of VEGFR-2, a receptor that mediates almost all of the known cellular responses to VEGF, while expression of VEGFR-1, a receptor that acts as a decoy receptor sequestering VEGF from VEGFR-2 binding, was at similar level in normal and GBM ECs (Fig. 1c), providing a possible mechanism for the anti-VEGF resistance in GBM ECs. This evidence concerns the gene KDR and neoplasm.