Author/Authors :
Fuereder، نويسنده , , Thorsten and Jaeger-Lansky، نويسنده , , Agnes and Hoeflmayer، نويسنده , , Doris and Preusser، نويسنده , , Matthias and Strommer، نويسنده , , Sabine and Cejka، نويسنده , , Daniel and Koehrer، نويسنده , , Stefan and Crevenna، نويسنده , , Richard and Wacheck، نويسنده , , Volker، نويسنده ,
Abstract :
VEGF receptor blockage has been reported to increase serum VEGF. We hypothesized that mTOR inhibition by everolimus counteracts VEGF induction by sunitinib resulting in an improved anti-tumor activity of sunitinib. In vitro, sunitinib in combination with everolimus did not outperform the respective monotherapies. In vivo, monotherapies reduced tumor growth by 60%, whereas the combination of sunitinib and everolimus led to an almost complete tumor growth inhibition. This superior anti-tumor activity coincided with attenuation of VEGF peaks. In conclusion mTOR inhibition by everolimus counteracts VEGF induction by sunitinib and results in significant reduction of tumor burden and long-lasting tumor growth control.
Keywords :
Gastric cancer , mTOR , VEGF , Angiogenesis , Sunitinib
