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Pharmacologic activation of tumor hypoxia: a means to increase tumor 2-deoxy-2-[18F]fluoro-D-glucose uptake?

(2013) MOLECULAR IMAGING. 12(1). p.49-58
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Abstract
Tumor hypoxia and tumor metabolism are linked through the activation of metabolic genes following hypoxia-inducible factor 1 (HIF-1) activation. This raises the question of whether this relationship can be exploited to improve 2-deoxy-2-[F-18]fluoro-D-glucose positron emission tomography ([F-18]FDG-PET). To do this, [F-18]FDG uptake was investigated after chemical induction of hypoxia and chemical activation of HIF-1 in an in vitro and an in vivo model of a human colorectal carcinoma. [F-18]FDG uptake, HIF-1 alpha protein levels, and messenger ribonucleic acid expression of glucose transporter 1 (GLUT1), hexokinase 2, HIF-1 alpha, and carbonic anhydrase IX (CA IX) were determined in HT29 cells after treatment with 200 mu M CoCl2 and 500 mu M dimethyloxalylglycine (DMOG). In an HT29 xenograft, the distribution of endogenous and exogenous markers of hypoxia was investigated using immunohistochemistry, and tumor [F-18]FDG uptake was determined after treatment with a single dose of 5 mg/kg hydralazine and 8 mg DMOG. Treatment of HT29 cells with CoCl2 and DMOG induced functional HIF-1 and resulted in increased [(18) F]FDG uptake. In an HT29 xenograft, a similar spatial distribution of pimonidazole, CA IX, and GLUT1 was found, and treatment with DMOG resulted in significant increases in maximum and mean standardized uptake values using [(18) F]FDG-PET. Chemical activation of HIF-1 can increase in vitro and in vivo [(18) F]FDG uptake. Imaging after pharmacologic HIF-1 activation might increase tumor [(18) F]FDG uptake when using [(18) F]FDG-PET.
Keywords
CANCER-CELLS, CARBONIC-ANHYDRASE-IX, IN-VITRO, GLUCOSE-TRANSPORTER, OXYGEN-TENSION, FDG UPTAKE, INHIBITION, EXPRESSION, HYDROXYLASES, ACCUMULATION

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Citation

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Chicago
Mees, Gilles, Rudi Dierckx, CHRISTEL VANGESTEL, Debby Laukens, Nancy Van Damme, and Christophe Van De Wiele. 2013. “Pharmacologic Activation of Tumor Hypoxia: a Means to Increase Tumor 2-deoxy-2-[18F]fluoro-D-glucose Uptake?” Molecular Imaging 12 (1): 49–58.
APA
Mees, G., Dierckx, R., VANGESTEL, C., Laukens, D., Van Damme, N., & Van De Wiele, C. (2013). Pharmacologic activation of tumor hypoxia: a means to increase tumor 2-deoxy-2-[18F]fluoro-D-glucose uptake? MOLECULAR IMAGING, 12(1), 49–58.
Vancouver
1.
Mees G, Dierckx R, VANGESTEL C, Laukens D, Van Damme N, Van De Wiele C. Pharmacologic activation of tumor hypoxia: a means to increase tumor 2-deoxy-2-[18F]fluoro-D-glucose uptake? MOLECULAR IMAGING. 2013;12(1):49–58.
MLA
Mees, Gilles, Rudi Dierckx, CHRISTEL VANGESTEL, et al. “Pharmacologic Activation of Tumor Hypoxia: a Means to Increase Tumor 2-deoxy-2-[18F]fluoro-D-glucose Uptake?” MOLECULAR IMAGING 12.1 (2013): 49–58. Print.
@article{4146868,
  abstract     = {Tumor hypoxia and tumor metabolism are linked through the activation of metabolic genes following hypoxia-inducible factor 1 (HIF-1) activation. This raises the question of whether this relationship can be exploited to improve 2-deoxy-2-[F-18]fluoro-D-glucose positron emission tomography ([F-18]FDG-PET). To do this, [F-18]FDG uptake was investigated after chemical induction of hypoxia and chemical activation of HIF-1 in an in vitro and an in vivo model of a human colorectal carcinoma. [F-18]FDG uptake, HIF-1 alpha protein levels, and messenger ribonucleic acid expression of glucose transporter 1 (GLUT1), hexokinase 2, HIF-1 alpha, and carbonic anhydrase IX (CA IX) were determined in HT29 cells after treatment with 200 mu M CoCl2 and 500 mu M dimethyloxalylglycine (DMOG). In an HT29 xenograft, the distribution of endogenous and exogenous markers of hypoxia was investigated using immunohistochemistry, and tumor [F-18]FDG uptake was determined after treatment with a single dose of 5 mg/kg hydralazine and 8 mg DMOG. Treatment of HT29 cells with CoCl2 and DMOG induced functional HIF-1 and resulted in increased [(18) F]FDG uptake. In an HT29 xenograft, a similar spatial distribution of pimonidazole, CA IX, and GLUT1 was found, and treatment with DMOG resulted in significant increases in maximum and mean standardized uptake values using [(18) F]FDG-PET. Chemical activation of HIF-1 can increase in vitro and in vivo [(18) F]FDG uptake. Imaging after pharmacologic HIF-1 activation might increase tumor [(18) F]FDG uptake when using [(18) F]FDG-PET.},
  author       = {Mees, Gilles and Dierckx, Rudi and VANGESTEL, CHRISTEL and Laukens, Debby and Van Damme, Nancy and Van De Wiele, Christophe},
  issn         = {1535-3508},
  journal      = {MOLECULAR IMAGING},
  keyword      = {CANCER-CELLS,CARBONIC-ANHYDRASE-IX,IN-VITRO,GLUCOSE-TRANSPORTER,OXYGEN-TENSION,FDG UPTAKE,INHIBITION,EXPRESSION,HYDROXYLASES,ACCUMULATION},
  language     = {eng},
  number       = {1},
  pages        = {49--58},
  title        = {Pharmacologic activation of tumor hypoxia: a means to increase tumor 2-deoxy-2-[18F]fluoro-D-glucose uptake?},
  url          = {http://dx.doi.org/10.2310/7290.2012.00020},
  volume       = {12},
  year         = {2013},
}

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