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Anti-VEGF
antibody treatment of glioblastoma prolongs survival but results
in increased vascular cooption
Rubenstein
JL, Kim J, Ozawa T, Zhang M, Westphal M, Deen DF, Shuman MA
Division
of Hematology/Oncology, University of California, San Francisco,
USA. jamesr@medicine.ucsf.edu
Vascular endothelial growth factor (VEGF) is an important mediator
of the intense angiogenesis which is characteristic of
glioblastoma.
While genetic manipulation of VEGF/VEGF receptor expression has
previously been shown to inhibit glioblastoma growth, to date, no
study has examined the efficacy of pharmacologic blockade of VEGF
activity as a means to inhibit intracranial growth of human
glioblastoma.
Using intraperitoneal administration of a neutralizing anti-VEGF
antibody, we demonstrate that inhibition of VEGF significantly
prolongs survival in athymic rats inoculated in the basal ganglia
with G55 human glioblastoma cells.
Systemic anti-VEGF inhibition causes decreased tumor vascularity
as well as a marked increase in tumor cell apoptosis in
intracranial tumors.
Although intracranial glioblastoma tumors grow more slowly as a
consequence of anti-VEGF treatment, the histologic pattern of
growth suggests that these tumors adapt to inhibition of
angiogenesis by increased infiltration and cooption of the host
vasculature.
PMID: 11005565 [PubMed - indexed for MEDLINE]
Source:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11005565&dopt=Abstract
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