{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:57Z","timestamp":1791331257813,"version":"4.3.1"},"reference-count":45,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,3,6]],"date-time":"2014-03-06T00:00:00Z","timestamp":1394064000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Contrast Media &amp; Molecular"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:p>The purpose of this study was to assess the effect of bevacizumab on vasculature and hypoxia in a colorectal tumor model. Nude mice with subcutaneous LS174T tumors were treated with bevacizumab or saline. To assess tumor properties, separate groups of mice were imaged using <jats:sup>18<\/jats:sup>F\u2010Fluoromisonidazole (FMISO) and <jats:sup>18<\/jats:sup>F\u2010Fluorodeoxyglucose (FDG) positron emission tomography or magnetic resonance imaging before and 2, 6 and 10\u2009days after the start of treatment. Tumors were harvested after imaging to determine hypoxia and vascular density immunohistochemically. The <jats:italic>T<\/jats:italic><jats:sub>2<\/jats:sub>* time increased significantly less in the bevacizumab group. FMISO uptake increased more over time in the control group. Vessel density significantly decreased in the bevacizumab\u2010treated group. The Carbonic anhydrase 9 (CAIX) and glucose uptake transporter 1 (GLUT1) fractions were higher in bevacizumab\u2010treated tumors. However, the hypoxic fraction showed no significant difference. Bevacizumab led to shorter <jats:italic>T<\/jats:italic><jats:sub>2<\/jats:sub>* times and higher GLUT1 and CAIX expression, suggesting an increase in hypoxia and a higher glycolytic rate. This could be a mechanism of resistance to bevacizumab. The increase in hypoxia, however, could not be demonstrated by pimonidazole\/FMISO, possibly because distribution of these tracers is hampered by bevacizumab\u2010induced effects on vascular permeability and perfusion. 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