期刊
CANCER RESEARCH
卷 72, 期 2, 页码 402-407出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-11-2464
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资金
- NCI/NIH [R21CA117079, R01CA129371, K24CA125440]
- NIH [S10RR023401, S10RR019307, S10RR019254, S10RR023043, S10RR021110, R01CA137254, 5R01NS060918, UL1 RR025758]
- NCI [P01CA80124]
- Saic-Frederick Inc. [26XS263]
- Norwegian Research Council [191088/V50]
- Harvard Catalyst grant [M01-RR-01066]
- Merck
- Sanofi-Aventis
- Genentech
- Novartis
- Medimmune
- AstraZeneca
- Amgen
- Vascular Biogenics
- Genzyme
- Millennium
- Pfizer
- Dyax
- Roche
The abnormal vasculature of the tumor microenvironment supports progression and resistance to treatment. Judicious application of antiangiogenic therapy may normalize the structure and function of the tumor vasculature, promoting improved blood perfusion. However, direct clinical evidence is lacking for improvements in blood perfusion after antiangiogenic therapy. In this study, we used MRI to assess tumor blood perfusion in 30 recurrent glioblastoma patients who were undergoing treatment with cediranib, a pan-VEGF receptor tyrosine kinase inhibitor. Tumor blood perfusion increased durably for more than 1 month in 7 of 30 patients, in whom it was associated with longer survival. Together, our findings offer direct clinical evidence in support of the hypothesis that vascular normalization can increase tumor perfusion and help improve patient survival. Cancer Res; 72(2); 402-7. (C)2011 AACR.
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