|1.||Ronen, Sabrina M: 1 article (06/2012)|
|2.||Burghardt, Andrew J: 1 article (06/2012)|
|3.||Dafni, Hagit: 1 article (06/2012)|
|4.||Navone, Nora M: 1 article (06/2012)|
|5.||Majumdar, Sharmila: 1 article (06/2012)|
|6.||Cherrington, Julie M: 1 article (05/2006)|
|7.||Barone, Angela: 1 article (05/2006)|
|8.||Mendel, Dirk B: 1 article (05/2006)|
|9.||Potapova, Olga: 1 article (05/2006)|
|10.||Moss, Katherine G: 1 article (05/2006)|
05/01/2006 - "SU10944 alone induced a tumor growth delay in all models evaluated, consistent with a primarily antiangiogenic mode of action. "
06/01/2012 - "Despite these structural differences, vascular permeability was reduced in both tumor models by either imatinib or SU10944 treatment. "
05/01/2006 - "Moreover, SU10944 combined with Gleevec inhibited tumor neoangiogenesis to an extent comparable to that of SU11248. "
05/01/2006 - "Strikingly, in all but one tumor model evaluated, the antitumor efficacy of SU10944 combined with Gleevec was similar to that of single-agent SU11248, and was greatly superior to that of each compound alone, indicating that the antitumor potency of SU11248 in these models stems from combined inhibition of both PDGF and VEGF receptors. "
|2.||Vascular Endothelial Growth Factor Receptors (VEGF Receptors)