| 1. |
- Amirian, E. Susan, et al.
(författare)
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Aspirin, NSAIDs, and Glioma Risk : Original Data from the Glioma International Case-Control Study and a Meta-analysis
- 2019
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : American Association for Cancer Research (AACR). - 1055-9965 .- 1538-7755. ; 28:3, s. 555-562
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Tidskriftsartikel (refereegranskat)abstract
- Background: There have been few studies of sufficient size to address the relationship between glioma risk and the use of aspirin or NSAIDs, and results have been conflicting. The purpose of this study was to examine the associations between glioma and aspirin/NSAID use, and to aggregate these findings with prior published studies using meta-analysis.Methods: The Glioma International Case-Control Study (GICC) consists of 4,533 glioma cases and 4,171 controls recruited from 2010 to 2013. Interviews were conducted using a standardized questionnaire to obtain information on aspirin/NSAID use. We examined history of regular use for ≥6 months and duration-response. Restricted maximum likelihood meta-regression models were used to aggregate site-specific estimates, and to combine GICC estimates with previously published studies.Results: A history of daily aspirin use for ≥6 months was associated with a 38% lower glioma risk, compared with not having a history of daily use [adjusted meta-OR = 0.62; 95% confidence interval (CI), 0.54–0.70]. There was a significant duration-response trend (P = 1.67 × 10−17), with lower ORs for increasing duration of aspirin use. Duration-response trends were not observed for NSAID use. In the meta-analysis aggregating GICC data with five previous studies, there was a marginally significant association between use of aspirin and glioma (mOR = 0.84; 95% CI, 0.70–1.02), but no association for NSAID use.Conclusions: Our study suggests that aspirin may be associated with a reduced risk of glioma.Impact: These results imply that aspirin use may be associated with decreased glioma risk. Further research examining the association between aspirin use and glioma risk is warranted.
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| 2. |
- Bainbridge, Matthew N, et al.
(författare)
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Germline mutations in shelterin complex genes are associated with familial glioma
- 2015
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press. - 0027-8874 .- 1460-2105. ; 107:1
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Tidskriftsartikel (refereegranskat)abstract
- Gliomas are the most common brain tumor, with several histological subtypes of various malignancy grade. The genetic contribution to familial glioma is not well understood. Using whole exome sequencing of 90 individuals from 55 families, we identified two families with mutations in POT1 (p.G95C, p.E450X), a member of the telomere shelterin complex, shared by both affected individuals in each family and predicted to impact DNA binding and TPP1 binding, respectively. Validation in a separate cohort of 264 individuals from 246 families identified an additional mutation in POT1 (p.D617Efs), also predicted to disrupt TPP1 binding. All families with POT1 mutations had affected members with oligodendroglioma, a specific subtype of glioma more sensitive to irradiation. These findings are important for understanding the origin of glioma and could have importance for the future diagnostics and treatment of glioma.
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| 3. |
- Jalali, Ali, et al.
(författare)
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Targeted sequencing in chromosome 17q linkage region identifies familial glioma candidates in the Gliogene Consortium
- 2015
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Ingår i: Scientific Reports. - : Nature Publishing Group. - 2045-2322. ; 5, s. 8278-
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Tidskriftsartikel (refereegranskat)abstract
- Glioma is a rare, but highly fatal, cancer that accounts for the majority of malignant primary brain tumors. Inherited predisposition to glioma has been consistently observed within non-syndromic families. Our previous studies, which involved non-parametric and parametric linkage analyses, both yielded significant linkage peaks on chromosome 17q. Here, we use data from next generation and Sanger sequencing to identify familial glioma candidate genes and variants on chromosome 17q for further investigation. We applied a filtering schema to narrow the original list of 4830 annotated variants down to 21 very rare (<0.1% frequency), non-synonymous variants. Our findings implicate the MYO19 and KIF18B genes and rare variants in SPAG9 and RUNDC1 as candidates worthy of further investigation. Burden testing and functional studies are planned.
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| 4. |
- Sotoudeh Anvari, Maryam, et al.
(författare)
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Relationship between calculated total antioxidant status and atherosclerotic coronary artery disease.
- 2016
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Ingår i: The Anatolian Journal of Cardiology. - 2149-2263 .- 2149-2271. ; 16:9, s. 689-695
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Antioxidants play a major role in the cellular protection cascade against oxidative damage. Oxidative stress has been linked to the pathogenesis of coronary atherosclerosis. Our aim was to evaluate the association between calculated serum total antioxidant status (cTAS) and the presence and severity of coronary artery disease (CAD).Methods: One hundred and seventy-four patients with angiographically documented significant (≥50%) luminal stenosis (n=123) or with minimal (<50%) luminal stenosis (n=51) in at least one coronary artery or major branch segment in the epicardial coronary tree were categorized as CAD+ group; 88 patients with no luminal stenosis were considered as the control group. The level of cTAS (mmol/L) was evaluated using the following equation: (0.63×albumin concentration)+(1.02×uric acid concentration)+(1.53×bilirubin concentration).Results: In univariate analyses, mean levels of cTAS, uric acid, and creatinine were significantly higher in CAD+ group than in controls. However, adjusted cTAS level was not found to be a CAD predictor in the total population [odds ratio (OR)=1.20; 95% confidence interval (CI): 0.81–1.76;p=0.364] or in men (OR=1.25; 95% CI: 0.73–2.12; p=0.420) and women (OR=1.20; 95% CI: 0.66–2.19; p=0.553). A weak but statistically significant correlation was found between cTAS and Gensini score (Spearman’s ρ=0.16, p=0.015).Conclusion: In patients with suspicious CAD, the level of cTAS was not found to be an independent predictor for the presence of CAD. Further studies with larger sample size are required to confirm the results.
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