The host site is believed to regulate
tumor angiogenesis, which could result in site-dependent
drug delivery parameters, greatly affecting experimental
tumor research. In RG-2 rat
gliomas we measured cellular proliferation; cell cycle time was the same for RG-2 cells in brain and s.c.
tumors (25 h), and was the same for endothelial cells in these
tumors (46 h). We measured the transcapillary transfer constant (K) of
alpha-aminoisobutyric acid and blood flow (F) with
iodoantipyrine in RG-2
gliomas transplanted into brain, liver, kidney, muscle, s.c. tissue, and into the abdominal cavity. Data was evaluated by quantitative autoradiography and direct tissue sampling. The variation of F (12.6-84.0 ml/g/min) and K (26.1-49.2 microl/g/min) in RG-2
tumors in the different host sites was less than in surrounding
tumor-free tissue (F = 20-1500 ml/g/min and K = 1.6-700 microl/g/min). In contrast to other models, RG-2 does not result in
tumors with host site-dependent behavior. The RG-2
tumor cells appear to participate in, if not dominate, the angiogenesis process regardless of the host site. Values of F and K were more dependent on
tumor topography (center versus periphery) and local histological features (
necrosis versus viable
tumor) than host site. We believe that the methods used for data acquisition may introduce as much variability in Results as the
tumors themselves and that to better understand how
tumor angiogenesis affects the vascular phenotype, comparative studies are needed to validate the results obtained with newer methodologies.