Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer.

Research output: Contribution to journalConference abstract in journalpeer-review

Standard

Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer. / Engelmann, Bodil E.; Binderup, Tina; Kjær, Andreas; Loft, Annika; Gerds, Thomas A.; Berthelsen, Anne Kiil; Brinch, Kim; Latocha, Jan E.; Sloth, Carsten; Højgaard, Liselotte.

In: Journal of Clinical Oncology, Vol. 33, No. 3, Supplement, 653, 20.01.2015.

Research output: Contribution to journalConference abstract in journalpeer-review

Harvard

Engelmann, BE, Binderup, T, Kjær, A, Loft, A, Gerds, TA, Berthelsen, AK, Brinch, K, Latocha, JE, Sloth, C & Højgaard, L 2015, 'Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer.', Journal of Clinical Oncology, vol. 33, no. 3, Supplement, 653. <http://meeting.ascopubs.org/cgi/content/abstract/33/3_suppl/653>

APA

Engelmann, B. E., Binderup, T., Kjær, A., Loft, A., Gerds, T. A., Berthelsen, A. K., Brinch, K., Latocha, J. E., Sloth, C., & Højgaard, L. (2015). Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer. Journal of Clinical Oncology, 33(3, Supplement), [653]. http://meeting.ascopubs.org/cgi/content/abstract/33/3_suppl/653

Vancouver

Engelmann BE, Binderup T, Kjær A, Loft A, Gerds TA, Berthelsen AK et al. Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer. Journal of Clinical Oncology. 2015 Jan 20;33(3, Supplement). 653.

Author

Engelmann, Bodil E. ; Binderup, Tina ; Kjær, Andreas ; Loft, Annika ; Gerds, Thomas A. ; Berthelsen, Anne Kiil ; Brinch, Kim ; Latocha, Jan E. ; Sloth, Carsten ; Højgaard, Liselotte. / Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer. In: Journal of Clinical Oncology. 2015 ; Vol. 33, No. 3, Supplement.

Bibtex

@article{8ecc99c3b90343ce9f53eeb3884a9b0b,
title = "Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer.",
abstract = "Background: Positron emission tomography (PET) with the glucose analogue 18F-fluorodeoxyglucose (FDG) is widely used in oncologic imaging. This study examines the molecular mechanism underlying the detection of colon cancer (CC) by FDG-PET. Methods: Pre-operative PET/CT scans and tissue samples from primary CC and surrounding normal mucosa were obtained from 42 patients. FDG uptake was quantified using maximal standardized uptake value (SUVmax). The expression of ki67, glucose transporter 1 (GLUT-1), hexokinase 1 (HK1), hexokinase 2 (HK2), vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α (HIF1α) and carbonic anhydrase IX (CaIX) mRNA was examined by quantitative real time reverse transcriptase-polymerase chain reaction. Results: All primary tumours showed increased uptake of FDG. The mean SUVmax was 15.0 (range 5.3 – 37.8). No correlation was found between tumour size and SUVmax. Mean gene expression levels of GLUT1, HK2, ki67, HIF1α, VEGF and CaIX, but not HK1, were significantly higher in primary tumours than in surrounding normal colonic mucosa. Linear regressions pairing tumour SUVmax with gene expression levels showed significant correlations between SUVmax and HK2, ki67 and CaIX, respectively. Conclusions: These results confirm FDG PET/CT as a functional imaging method in CC, and that FDG accumulation reflects molecular events related to glycolysis, cell proliferation, hypoxia, but not angiogenesis.",
author = "Engelmann, {Bodil E.} and Tina Binderup and Andreas Kj{\ae}r and Annika Loft and Gerds, {Thomas A.} and Berthelsen, {Anne Kiil} and Kim Brinch and Latocha, {Jan E.} and Carsten Sloth and Liselotte H{\o}jgaard",
year = "2015",
month = jan,
day = "20",
language = "English",
volume = "33",
journal = "Journal of Clinical Oncology",
issn = "0732-183X",
publisher = "American Society of Clinical Oncology",
number = "3, Supplement",

}

RIS

TY - ABST

T1 - Quantitative gene expression underlying 18f-fluorodeoxyglucose uptake in colon cancer.

AU - Engelmann, Bodil E.

AU - Binderup, Tina

AU - Kjær, Andreas

AU - Loft, Annika

AU - Gerds, Thomas A.

AU - Berthelsen, Anne Kiil

AU - Brinch, Kim

AU - Latocha, Jan E.

AU - Sloth, Carsten

AU - Højgaard, Liselotte

PY - 2015/1/20

Y1 - 2015/1/20

N2 - Background: Positron emission tomography (PET) with the glucose analogue 18F-fluorodeoxyglucose (FDG) is widely used in oncologic imaging. This study examines the molecular mechanism underlying the detection of colon cancer (CC) by FDG-PET. Methods: Pre-operative PET/CT scans and tissue samples from primary CC and surrounding normal mucosa were obtained from 42 patients. FDG uptake was quantified using maximal standardized uptake value (SUVmax). The expression of ki67, glucose transporter 1 (GLUT-1), hexokinase 1 (HK1), hexokinase 2 (HK2), vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α (HIF1α) and carbonic anhydrase IX (CaIX) mRNA was examined by quantitative real time reverse transcriptase-polymerase chain reaction. Results: All primary tumours showed increased uptake of FDG. The mean SUVmax was 15.0 (range 5.3 – 37.8). No correlation was found between tumour size and SUVmax. Mean gene expression levels of GLUT1, HK2, ki67, HIF1α, VEGF and CaIX, but not HK1, were significantly higher in primary tumours than in surrounding normal colonic mucosa. Linear regressions pairing tumour SUVmax with gene expression levels showed significant correlations between SUVmax and HK2, ki67 and CaIX, respectively. Conclusions: These results confirm FDG PET/CT as a functional imaging method in CC, and that FDG accumulation reflects molecular events related to glycolysis, cell proliferation, hypoxia, but not angiogenesis.

AB - Background: Positron emission tomography (PET) with the glucose analogue 18F-fluorodeoxyglucose (FDG) is widely used in oncologic imaging. This study examines the molecular mechanism underlying the detection of colon cancer (CC) by FDG-PET. Methods: Pre-operative PET/CT scans and tissue samples from primary CC and surrounding normal mucosa were obtained from 42 patients. FDG uptake was quantified using maximal standardized uptake value (SUVmax). The expression of ki67, glucose transporter 1 (GLUT-1), hexokinase 1 (HK1), hexokinase 2 (HK2), vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α (HIF1α) and carbonic anhydrase IX (CaIX) mRNA was examined by quantitative real time reverse transcriptase-polymerase chain reaction. Results: All primary tumours showed increased uptake of FDG. The mean SUVmax was 15.0 (range 5.3 – 37.8). No correlation was found between tumour size and SUVmax. Mean gene expression levels of GLUT1, HK2, ki67, HIF1α, VEGF and CaIX, but not HK1, were significantly higher in primary tumours than in surrounding normal colonic mucosa. Linear regressions pairing tumour SUVmax with gene expression levels showed significant correlations between SUVmax and HK2, ki67 and CaIX, respectively. Conclusions: These results confirm FDG PET/CT as a functional imaging method in CC, and that FDG accumulation reflects molecular events related to glycolysis, cell proliferation, hypoxia, but not angiogenesis.

M3 - Conference abstract in journal

VL - 33

JO - Journal of Clinical Oncology

JF - Journal of Clinical Oncology

SN - 0732-183X

IS - 3, Supplement

M1 - 653

ER -

ID: 161782039