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into Established Brain Tumors Represses Growth by Antiangiogenesis
Departments of
*
Neurology and
Anesthesia and Pain Management, and
Center for Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75235
The experiments in this paper were designed to examine the
therapeutic effects of adenoviral-mediated gene transfer of IFN-
into a mouse model of an established metastatic brain tumor.
Temperature-sensitive replication-defective adenovirus was generated
for gene transfer of IFN- (AdIFN) and ß-galactosidase (AdBGAL)
cDNAs in vivo. In this model, treatment with AdIFN elicits prolonged
survival times and brain tumor rejection. Evidence against an
immune-mediated response accounting for this result include: 1) absence
of a memory immune response upon challenge, 2) lack of antitumor
effects at sites distal to inoculation of AdIFN, and 3) preservation of
the therapeutic effects of AdIFN in scid and beige mice
and in inducible NO synthase (iNOS) knockouts. High concentrations of
IFN- do not inhibit tumor growth in vitro making it unlikely that
the antitumor effect of this treatment acts directly on the growth of
the tumor cells. However, gene transfer of IFN- inhibits
neovascularization of the tumor in a 3LL-Matrigel assay in vivo, and
AdIFN induces apoptosis of endothelial cells in vivo, supporting the
idea that AdIFN represses tumor growth by inhibiting angiogenesis. The
substantial non-immune-mediated therapeutic benefits of AdIFN in
animals paves the way for devising novel strategies for treating human
brain tumors.
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