Vascular endothelial growth factor (VEGF) receptor antibody bevacizumab (avastin) induces regression of renal cell carcinoma in an adolescent resulting in residual tumorectomy

2008 ◽  
Vol 50 (4) ◽  
pp. 903-904 ◽  
Author(s):  
Divya-Devi Joshi ◽  
Tarit Banerjee
Keyword(s):  
Renal Cell Carcinoma ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Receptor Antibody ◽  
Endothelial Growth Factor

Targeting vascular endothelial growth factor (VEGF)-receptor-signaling in renal cell carcinoma

2007 ◽  
Vol 25 (1) ◽  
pp. 59-72 ◽  
Author(s):  
Christoph W. M. Reuter ◽  
Michael A. Morgan ◽  
Viktor Grünwald ◽  
Thomas R. W. Herrmann ◽  
Martin Burchardt ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Receptor Signaling ◽  
Endothelial Growth Factor

scholarly journals BEST: A Randomized Phase II Study of Vascular Endothelial Growth Factor, RAF Kinase, and Mammalian Target of Rapamycin Combination Targeted Therapy With Bevacizumab, Sorafenib, and Temsirolimus in Advanced Renal Cell Carcinoma—A Trial of the ECOG–ACRIN Cancer Research Group (E2804)

2015 ◽  
Vol 33 (21) ◽  
pp. 2384-2391 ◽  
Author(s):  
Keith T. Flaherty ◽  
Judith B. Manola ◽  
Michael Pins ◽  
David F. McDermott ◽  
Michael B. Atkins ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Progression Free Survival ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Free Survival ◽  
Endothelial Growth Factor

Purpose On the basis of evidence that resistance to vascular endothelial growth factor (VEGF) receptor inhibition is caused by hypoxia-driven residual VEGF and other proangiogenic factors, combinations of agents from these classes were hypothesized to improve treatment outcomes relative to single-agent VEGF pathway blockade. Patients and Methods A total of 361 patients with metastatic clear cell renal cell carcinoma were randomly assigned equally to arm A (bevacizumab monotherapy 10 mg/kg intravenously [IV] every 2 weeks), B (bevacizumab 10 mg/kg IV every 2 weeks and temsirolimus 25 mg IV every week), C (bevacizumab 5 mg/kg IV every 2 weeks and sorafenib 200 mg orally twice daily on days 1 to 5, 8 to 12, 15 to 19, and 22 to 26), or D (sorafenib 200 mg twice daily and temsirolimus 25 mg IV weekly). Progression-free survival was the primary end point. Results Among 331 eligible treated patients, median PFS was 7.5 months for bevacizumab alone (90% CI, 5.8 to 10.8 months), 7.6 months for bevacizumab plus temsirolimus (90% CI, 6.7 to 9.2 months), 9.2 months for bevacizumab plus sorafenib (90% CI, 7.5 to 11.4 months), and 7.4 months for sorafenib plus temsirolimus (90% CI, 5.6 to 7.9 months). Hazard ratios from stratified Cox proportional hazards models were 1.01, 0.89, and 1.07 (with respective P values of .95, .49, and .68) for the three combinations, respectively, compared with bevacizumab alone. Adverse events did not differ significantly among treatment arms. Conclusion The activity of sorafenib, temsirolimus, and bevacizumab administered in doublet combinations did not significantly improve median progression-free survival in comparison with bevacizumab monotherapy.

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