Abstract
No strong aetiological factors have been established for glioma aside from genetic mutations and variants, ionising radiation and an inverse relationship with asthmas and allergies. Our aim was to investigate the association between pre‐diagnostic immune protein levels and glioma risk. We conducted a case–control study nested in the Northern Sweden Health and Disease Study cohort. We analysed 133 glioma cases and 133 control subjects matched by age, sex and date of blood donation. ELISA or Luminex bead‐based multiplex assays were used to measure plasma levels of 19 proteins. Conditional logistic regression models were used to estimate the odds ratios and 95% CIs. To further model the protein trajectories over time, the linear mixed‐effects models were conducted. We found that the levels of sVEGFR2, sTNFR2, sIL‐2Rα and sIL‐6R were associated with glioma risk. After adjusting for the time between blood sample collection and glioma diagnosis, the odds ratios were 1.72 (95% CI = 1.01–2.93), 1.48 (95% CI = 1.01–2.16) and 1.90 (95% CI = 1.14–3.17) for sTNFR2, sIL‐2Rα and sIL‐6R, respectively. The trajectory of sVEGFR2 concentrations over time was different between cases and controls (p‐value = 0.031), increasing for cases (0.8% per year) and constant for controls. Our findings suggest these proteins play important roles in gliomagenesis.
Highlights
Gliomas, the most frequent primary brain tumours, include glioblastoma (GBM), the most common and aggressive subtype with a median overall survival of14–17 months
Statistically significant associations with risk of glioma were found for soluble vascular endothelial growth factor receptor 2 (sVEGFR2), sIL-2Rα, soluble tumour necrosis factor receptor 2 (sTNFR2) and soluble interleukin 6 receptor (sIL-6R) (Table 3)
After adjusting for the sample collection time, the odds ratios (ORs) were 1.72, 1.48 and 1.90 for sTNFR2, sIL-2Rα and sIL-6R, respectively
Summary
The most frequent primary brain tumours, include glioblastoma (GBM), the most common and aggressive subtype with a median overall survival of14–17 months. |2 asthma and allergies and glioma risk, potentially indicating subtle immune dysregulation is involved in glioma development.[3] Studies over the past two decades have provided important information on the role of the immune system in gliomagenesis.[4] As cytokines are chemical messengers that regulate the innate and adaptive immune systems, the interaction with their receptors which can affect proliferation, angiogenesis and aggressiveness–– might play an important role in glioma progression.[5,6] Interestingly, haematological malignancies and glioma have some common aetiological pathways, such as exposure to ionising radiation and an inverse relationship with asthma and allergies.[7] In lymphoma studies, analysis of several relevant proteins, including sCD23, sCD27, sCD30 and CXCL13, in pre-diagnostic plasma samples have shown a significant difference between cases and controls even several years before diagnosis.[8,9] little is known about how the subclinical immunologic perturbations influence glioma risk. To gain further insight into the patterns of immune proteins in gliomagenesis according to the time between blood sample collection and glioma diagnosis, we investigated the protein trajectories over time in cases and controls
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