In vivo observation of intracellular oximetry in perfluorocarbon-labeled glioma cells and chemotherapeutic response in the CNS using fluorine-19 MRI
✍ Scribed by Deepak K. K. Kadayakkara; Jelena M. Janjic; Lisa K. Pusateri; Won-Bin Young; Eric T. Ahrens
- Book ID
- 102533989
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 354 KB
- Volume
- 64
- Category
- Article
- ISSN
- 0740-3194
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✦ Synopsis
Abstract
Preclinical development of therapeutic agents against cancer could greatly benefit from noninvasive markers of tumor killing. Potentially, the intracellular partial pressure of oxygen (pO~2~) can be used as an early marker of antitumor efficacy. Here, the feasibility of measuring intracellular pO~2~ of central nervous system glioma cells in vivo using ^19^F magnetic resonance techniques is examined. Rat 9L glioma cells were labeled with perfluoro‐15‐crown‐5‐ether ex vivo and then implanted into the rat striatum. ^19^F MRI was used to visualize tumor location in vivo. The mean ^19^F T~1~ of the implanted cells was measured using localized, single‐voxel spectroscopy. The intracellular pO~2~ in tumor cells was determined from an in vitro calibration curve. The basal pO~2~ of 9L cells (day 3) was determined to be 45.3 ± 5 mmHg (n = 6). Rats were then treated with a 1× LD10 dose of bischloroethylnitrosourea intravenously and changes in intracellular pO~2~ were monitored. The pO~2~ increased significantly (P = 0.042, paired T‐test) to 141.8 ± 3 mmHg within 18 h after bischloroethylnitrosourea treatment (day 4) and remained elevated (165 ± 24 mmHg) for at least 72 h (day 6). Intracellular localization of the perfluoro‐15‐crown‐5‐ether emulsion in 9L cells before and after bischloroethylnitrosourea treatment was confirmed by histological examination and fluorescence microscopy. Overall, noninvasive ^19^F magnetic resonance techniques may provide a valuable preclinical tool for monitoring therapeutic response against central nervous system or other deep‐seated tumors. Magn Reson Med, 2010. © 2010 Wiley‐Liss, Inc.