Ghent University Academic Bibliography

Advanced

Carbonic anhydrase IX expression correlates with FDG uptake by primary non-small cell lung cancer

Gilles Mees UGent, CHRISTEL VANGESTEL UGent, Rudi Dierckx UGent, Patrick Pauwels UGent, Jan Van Meerbeeck UGent and Christophe Van De Wiele UGent (2010) CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS. 25(2). p.149-154
abstract
Tumor cells are characterized by an increased rate of glucose consumption and glycolysis. This increased glucose consumption leads to tumor acidification, which represents a major obstacle for several therapeutic strategies. Tumor cells have adapted to this acidification by upregulation of several H+-extruding transporter systems and proteins to cope with this compromised situation. One of these proteins is carbonic anhydrase IX (CA IX), which catalyzes the reversible hydration of carbon dioxide to carbonic acid outside the cell, leading to an acidic extracellular pH and a physiological intracellular pH. The aim of this article was to study semiquantitatively the expression of CA IX in non-small cell lung cancer (NSCLC) and to assess the existence of a possible relationship between CA IX expression and tumor FDG uptake, reflecting glucose metabolism. The levels and the extent of CA IX expression were estimated in immunohistochemical stained, formalin-fixed, paraffin-embedded tissue samples from 18 patients with NSCLC and compared with FDG uptake in FDG-PET imaging. We found a statistically significant correlation between CA IX Hscores and SUVmax and SUVmean values of the primary tumor. This relationship provides indirect evidence for cotranscription of glucose transporters and hexokinases that drive tumor hyperglycolysis and for CA IX governed by hypoxia-inducible factor-1 and suggests that, in the future, it may be possible to identify NSCLC patients who are most likely to benefit from CA IX targeting therapy on the basis of FDG-PET imaging.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
pH, TUMOR HYPOXIA, NSCLC, FDG-PET, POOR-PROGNOSIS, CA IX, MARKER, CARBONIC-ANHYDRASE-9, SURVIVAL, THERAPY, PH, PROGRESSION, CARCINOMA, GROWTH
journal title
CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS
Cancer Biother. Radiopharm.
volume
25
issue
2
pages
149 - 154
Web of Science type
Article
Web of Science id
000277155900003
JCR category
RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING
JCR impact factor
1.873 (2010)
JCR rank
56/111 (2010)
JCR quartile
3 (2010)
ISSN
1084-9785
DOI
10.1089/cbr.2009.0658
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1262044
handle
http://hdl.handle.net/1854/LU-1262044
date created
2011-06-14 14:36:44
date last changed
2011-06-15 10:57:55
@article{1262044,
  abstract     = {Tumor cells are characterized by an increased rate of glucose consumption and glycolysis. This increased glucose consumption leads to tumor acidification, which represents a major obstacle for several therapeutic strategies. Tumor cells have adapted to this acidification by upregulation of several H+-extruding transporter systems and proteins to cope with this compromised situation. One of these proteins is carbonic anhydrase IX (CA IX), which catalyzes the reversible hydration of carbon dioxide to carbonic acid outside the cell, leading to an acidic extracellular pH and a physiological intracellular pH. The aim of this article was to study semiquantitatively the expression of CA IX in non-small cell lung cancer (NSCLC) and to assess the existence of a possible relationship between CA IX expression and tumor FDG uptake, reflecting glucose metabolism. The levels and the extent of CA IX expression were estimated in immunohistochemical stained, formalin-fixed, paraffin-embedded tissue samples from 18 patients with NSCLC and compared with FDG uptake in FDG-PET imaging. We found a statistically significant correlation between CA IX Hscores and SUVmax and SUVmean values of the primary tumor. This relationship provides indirect evidence for cotranscription of glucose transporters and hexokinases that drive tumor hyperglycolysis and for CA IX governed by hypoxia-inducible factor-1 and suggests that, in the future, it may be possible to identify NSCLC patients who are most likely to benefit from CA IX targeting therapy on the basis of FDG-PET imaging.},
  author       = {Mees, Gilles and VANGESTEL, CHRISTEL and Dierckx, Rudi and Pauwels, Patrick and Van Meerbeeck, Jan and Van De Wiele, Christophe},
  issn         = {1084-9785},
  journal      = {CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS},
  keyword      = {pH,TUMOR HYPOXIA,NSCLC,FDG-PET,POOR-PROGNOSIS,CA IX,MARKER,CARBONIC-ANHYDRASE-9,SURVIVAL,THERAPY,PH,PROGRESSION,CARCINOMA,GROWTH},
  language     = {eng},
  number       = {2},
  pages        = {149--154},
  title        = {Carbonic anhydrase IX expression correlates with FDG uptake by primary non-small cell lung cancer},
  url          = {http://dx.doi.org/10.1089/cbr.2009.0658},
  volume       = {25},
  year         = {2010},
}

Chicago
Mees, Gilles, CHRISTEL VANGESTEL, Rudi Dierckx, Patrick Pauwels, Jan Van Meerbeeck, and Christophe Van De Wiele. 2010. “Carbonic Anhydrase IX Expression Correlates with FDG Uptake by Primary Non-small Cell Lung Cancer.” Cancer Biotherapy and Radiopharmaceuticals 25 (2): 149–154.
APA
Mees, G., VANGESTEL, C., Dierckx, R., Pauwels, P., Van Meerbeeck, J., & Van De Wiele, C. (2010). Carbonic anhydrase IX expression correlates with FDG uptake by primary non-small cell lung cancer. CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS, 25(2), 149–154.
Vancouver
1.
Mees G, VANGESTEL C, Dierckx R, Pauwels P, Van Meerbeeck J, Van De Wiele C. Carbonic anhydrase IX expression correlates with FDG uptake by primary non-small cell lung cancer. CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS. 2010;25(2):149–54.
MLA
Mees, Gilles, CHRISTEL VANGESTEL, Rudi Dierckx, et al. “Carbonic Anhydrase IX Expression Correlates with FDG Uptake by Primary Non-small Cell Lung Cancer.” CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS 25.2 (2010): 149–154. Print.