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ARTICLE
Human glioma tumors express high levels of the chemokine receptor CX3CR1
1 Neurosurgery, Fondazione IRCCS, Ca’Granda Ospedale Maggiore Policlinico Mangiagalli e Regina Elena, Milan
2 II Cattedra di Anatomia Patologica, Dipartimento di Medicina, Chirurgia e Odontoiatria, University of Milan, A.O. San Paolo Milan
3 Institute of Experimental Neurology (INSPE), Scientific Institute San Raffaele, Milan
4 Department of Neurological Sciences, University of Milan
5 Istituto Clinico Humanitas IRCCS, Rozzano, Milan
6 Department of Translational Medicine, University of Milan, Italy
* Corresponding Author: A. Mantovani,
European Cytokine Network 2010, 21(1), 27-33. https://doi.org/10.1684/ecn.2009.0184
Accepted 08 December 2009;
Abstract
The chemokine receptor CX3CR1 and its cognate ligand CX3CL1 (also known as fractalkine), are involved in central nervous system pathophysiology, in particular, in the cross-talk between neurons and micro-glia. It was therefore important to investigate the expression of CX3CR1 in gliomas, the most frequently occur-ring, malignant brain tumors. In a consecutive series of 70 patients with primary, central nervous glial tumors, CX3CR1 was highly expressed in tumor cells as assessed by RT-PCR mRNA and protein levels, and by immu-nohistochemistry, while the corresponding normal cells were negative. Receptor immuno-positivity did not correlate with histology, grade, chromosomal (1p,19q) deletion, or with methylation of the DNA repair gene promoter MGMT (O6-methylguanine-DNA methyltransferase). Thus, CX3CR1 expression is a frequent event in gliomas, irrespective of tumor classification and clinical severity. The molecular basis underlying CX3CR1 up-regulation and its functional biological significance remain to be determined.Keywords
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Copyright © 2010 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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