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Background: A number of studies have investigated the roles of excision repair cross complementation group 1 (ERCC1), ERCC2, and ERCC5 genes polymorphisms in the development of glioma; however, the results were inconsistent. Here, we performed a meta-analysis to investigate the association between 6 polymorphisms in the ERCC genes (rs3212986, rs11615, rs13181, rs1799793, rs238406, rs17655) and glioma risk., Methods: The PubMed, Embase, and Web of science were searched up to September 6, 2016, for studies on the association between ERCC polymorphisms and glioma risk. A fixed-effects or random-effects model was used to calculate the pooled odds ratios based on the results from the heterogeneity tests. Sensitivity and cumulative meta-analyses were also performed., Results: A total of 15 studies were eligible for the pooled analysis, conducted in 2 populations of ethnic descent: 8 Europeans and 7 Asians. The results showed that ERCC1 rs3212986 polymorphism was positively associated with glioma [AA vs CC: odds ratio (OR) = 1.298, 95% confidence interval (95% CI) = 1.043-1.230, P = .025]. Association of the ERCC2 rs13181 and rs1799793 polymorphisms was only observed in Asians (CC vs AA for rs13181: OR = 1.539, 95% CI = 1.122-2.109, P = .007; AA vs GG for rs1799793: OR = 1.474, 95% CI = 1.090-1.994, P = .012). However, no association was observed between glioma risk and ERCC1 rs11615, ERCC2 rs238406, and ERCC5 rs17655 polymorphisms. Moreover, sensitivity and cumulative meta-analyses confirmed the stability of the results., Conclusions: Our meta-analysis indicated that the ERCC1 rs3212986 polymorphism and 2 polymorphisms in ERCC2 gene (rs13181 and rs1799793) contributed to the susceptibility of glioma.

Purpose: This study aimed to test prospectively whether exercise is associated with lower brain cancer mortality in 111,266 runners and 42,136 walkers from the National Runners' and Walkers' Health Studies., Methods: Hazard ratios and 95% confidence intervals (95% CI) from Cox proportional hazards analyses of mortality versus metabolic equivalent hours per day of exercise (MET-hours per day, where 1 MET = 3.5 mL O2·kg·min, or approximately 1-km run)., Results: The National Death Index identified 110 brain cancer deaths during an 11.7-yr average follow-up. Runners and walkers were combined because the brain cancer risk reduction did not differ significantly between MET-hours per day run and MET-hours per day walked (P = 0.66). When adjusted for sex, age, race, education, and cohort effects, the risk for brain cancer mortality was 43.2% lower for those who exercised 1.8 to 3.5 MET·h·d (95% CI = 2.6%-66.8% lower, P = 0.04) and 39.8% lower for those who exercised ≥ 3.6 MET·h·d (95% CI = 0.0%-64.0% lower, P = 0.05) compared with <1.8 MET·h·d at baseline. Pooling the runners and walkers who expended ≥ 1.8 MET·h·d showed a 42.5% lower risk of brain cancer mortality for the entire sample (95% CI: 8.0 to 64.1, P = 0.02) and 40.0% lower risk when three deaths that occurred within 1 yr of the baseline survey were excluded (95% CI = 1.3%-62.4%, P = 0.04)., Conclusions: The risk for fatal brain cancer decreased in association with running and walking energy expenditure. Our ability to detect an exercise-brain cancer relationship may relate to the use of cohorts specifically designed to detect exercise-health associations, and the calculation of exercise energy expenditure from kilometers per day walked and run rather than time spent exercising.

The authors propose "decreased-dose-intensity" PCV (procarbazine, lomustine [CCNU], and vincristine) chemotherapy for Asian patients with oligodendroglial tumors. In this study, all seven patients with oligodendroglioma (OD) and eight with anaplastic oligodendroglioma (AO) had objective responses or stable disease. Median progression-free survival was greater than 29 months (OD) and 36.5 months or greater (AO); 86% of patients with OD and 63% with AO remain progression-free. Twenty-four Common Toxicity Criteria Grade 3/4 adverse events were noted.

Objective: To determine with greater precision the map location of the locus associated with familial cavernous hemangiomas., Background: Cavernous malformations of the brain are a significant cause of seizures, progressive or apoplectic neurologic deficit, and headache. Prevalence estimates from autopsy series vary from 0.39 to 0.9%. This disorder (OMIM #116860) can be inherited as an autosomal dominant trait with variable penetrance. Linkage to markers on the long arm of chromosome 7 was recently reported in separate reports in three apparently unrelated Hispanic kindreds as well as in two kindreds of non-Hispanic descent., Design/methods: We examined clinically, by MRI scanning, and by pathologic examination of surgical specimens, members of four large Mexican-American families segregating cavernous hemangiomas of the brain. Linkage analysis was performed with use of blood specimens from morphologically proven cases. Two-point linkage analysis was performed with the MLINK program of the LINKAGE package. Multipoint analysis was performed between two markers and the disease locus with LINKMAP in the FASTLINKAGE package. Allele frequencies were set as described by the Genome Database (GDB). Maximum penetrance for the disease allele was set to 0.75., Results: The highest lod score was observed for marker D7S652 with Zmax = 6.66 at theta(max) = 0.00. Multipoint LOD score analysis placed the disease locus in the 11 cM interval between markers D7S630 and D7S527 with Zmax = 9.19. Haplotype analysis is in agreement with the placement of the disease gene between D7S630 and D7S527 and further shows a minimal shared region within this interval, indicating a founder effect in the establishment of the mutation in these families., Conclusions: We confirmed the linkage of cavernous hemangioma to markers on the long arm of chromosome 7q, and the estimate of the map location has been refined to a region of shared haplotype between markers D7S630 and D7S527 in four Mexican-American families who may be descended from a common ancestor in Sonora County, Mexico.