R1-dispersion profiles of in vivo glioma mouse models acquired by Fast-Field-Cycling NMR (FFC-NMR) were found to discriminate invasion from proliferation at fields below 2mT. These differences were correlated to the transcytolemmal water-exchange, demonstrating the water cell influx/outflux role in relaxation mechanisms. Hypoxia and H2O2, two major pathophysiological processes of invasion, were demonstrated to modulate relaxation. Immunohistochemistry of aquaporins AQP1 and AQP4 showed that the water-channel proteins were overexpressed in invasion but not in proliferation, suggesting that relaxations at low-field are modulated by water-exchange under the AQP1 and AQP4 control. The method can be extended to FFC imaging.
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