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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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MLA
Mees, Gilles, et al. “Pharmacologic Activation of Tumor Hypoxia: A Means to Increase Tumor 2-Deoxy-2-[18F]Fluoro-D-Glucose Uptake?” MOLECULAR IMAGING, vol. 12, no. 1, 2013, pp. 49–58, doi:10.2310/7290.2012.00020.
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. https://doi.org/10.2310/7290.2012.00020
Chicago author-date
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. https://doi.org/10.2310/7290.2012.00020.
Chicago author-date (all authors)
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. doi:10.2310/7290.2012.00020.
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.
IEEE
[1]
G. Mees, R. Dierckx, C. VANGESTEL, D. Laukens, N. Van Damme, and C. Van De Wiele, “Pharmacologic activation of tumor hypoxia: a means to increase tumor 2-deoxy-2-[18F]fluoro-D-glucose uptake?,” MOLECULAR IMAGING, vol. 12, no. 1, pp. 49–58, 2013.
@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}},
  keywords     = {{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://doi.org/10.2310/7290.2012.00020}},
  volume       = {{12}},
  year         = {{2013}},
}

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