1. Complement activation in Glioblastoma Multiforme pathophysiology: Evidence from serum levels and presence of complement activation products in tumor tissue
- Author
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T.A.M. Bouwens, Robert Veerhuis, Martine L.M. Lamfers, Clemens M F Dirven, Leendert A. Trouw, H. Al-Khawaja, Laboratory Medicine, Psychiatry, CCA - Disease profiling, and Neurosurgery
- Subjects
Adult ,Male ,Complement system ,Immunology ,Clinical Neurology ,chemical and pharmacologic phenomena ,Inflammation ,Enzyme-Linked Immunosorbent Assay ,Glial tumor ,Biology ,urologic and male genital diseases ,Complement factor B ,Mannose-Binding Lectin ,medicine ,Humans ,Immunology and Allergy ,Factor B ,Complement Activation ,C1q ,Effector ,Brain Neoplasms ,Complement C1q ,Middle Aged ,MBL deficiency ,medicine.disease ,Survival Analysis ,Pathophysiology ,Neurology ,Immunohistochemistry ,Mannose Binding Lectin (MBL) ,Female ,Neurology (clinical) ,medicine.symptom ,Glioblastoma ,Glioblastoma Multiforme ,Complement Factor B - Abstract
Inflammation plays a key role in the pathophysiology of Glioblastoma Multiforme (GBM). Here we focus on the contribution of the so far largely ignored complement system. ELISA and immunohistochemistry were combined to assess levels and localization of critical components of the initiation- and effector pathways of the complement cascade in sera and tumor tissue from GBM patients and matched controls. Serum levels of factor-B were decreased in GBM patients whereas C1q levels were increased. C1q and factor-B deposited in the tumor tissue. Deposition of C3 and C5b-9 suggests local complement activation. MBL deficiency, based on serum levels, was significantly less frequent among GBM patients compared to controls (14% vs. 33%). Therefore low levels of MBL may protect against the initiation/progression of GBM. (C) 2014 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).
- Published
- 2015
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