Genetic variants in telomerase-related genes are associated with an older age at diagnosis in glioma patients: evidence for distinct pathways of gliomagenesis

Walsh, Kyle M.; Rice, Terri; Decker, Paul A.; Kosel, Matthew L.; Kollmeyer, Thomas M.; Hansen, Helen M.; Zheng, Shichun; McCoy, Lucie; Bracci, Paige M.; Anderson, Erik L.; Hsuang, George; Wiemels, Joe; Pico, Alexander R.; Смирнов, Иван; Molinaro, Annette M.; Tihan, Tarık; Berger, Mitchell S.; Chang, Susan M.; Prados, Michael D.; Lachance, Daniel H.; Sicotte, Hugues; Eckel‐Passow, Jeanette E.; Wiencke, John K.; Jenkins, Robert B.; Wrensch, Margaret

doi:10.1093/neuonc/not051

Cited by 44 publications

(55 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gliomas account for approximately 80% of central nervous system malignant tumors and have a very poor prognosis (Schoemaker et al, 2010;Walsh et al, 2013b). Although the etiology of gliomas remains unclear, exposure to ionizing radiation has been identified as the only established risk factor (Little et al, 1998;Neglia et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…The gene polymorphisms increased or decreased glioma sensibility by regulating the proliferation and apoptosis of cells (Das et al, 2013;Liang et al, 2013). (Das et al, 2013;Li et al, 2013b) (Shete et al, 2009;Wrensch et al, 2009;Jin et al, 2013;Li et al, 2013;Walcott et al, 2013;Walsh et al, 2013a;Walsh et al, 2013b). Several research groups have reported associations between the rs6010620 single nucleotide polymorphism (SNP) and glioma risk.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The RTEL1 rs6010620 Polymorphism and Glioma Risk: a Meta-analysis Based on 12 Case-control Studies

Geng²,

Tian³

et al. 2015

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Background: The association between the RTEL1 rs6010620 single nucleotide polymorphism (SNP) and glioma risk has been extensively studied. However, the results remain inconclusive. To further examine this association, we performed a meta-analysis. Materials and Methods: A computerized search of the PubMed and Embase databases for publications regarding the RTEL1 rs6010620 polymorphism and glioma cancer risk was performed. Genotype data were analyzed in a meta-analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association. Sensitivity analyses, tests of heterogeneity, cumulative meta-analyses, and assessments of bias were performed in our meta-analysis. Results: Our meta-analysis confirmed that risk with allele A is lower than with allele G for glioma. In all genetic models, the association between the RTEL1 rs6010620 polymorphism and glioma risk was significant. This meta-analysis suggests that the RTEL1 rs6010620 polymorphism may be a risk factor for glioma. Further functional studies evaluating this polymorphism and glioma risk are warranted.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The RTEL1 rs6010620 Polymorphism and Glioma Risk: a Meta-analysis Based on 12 Case-control Studies

Geng²,

Tian³

et al. 2015

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

show abstract

“…The CCDC26 gene locus was strongly associated with glioma through five SNPs including rs4295627, rs16904140, rs6470745, rs891835, and rs10464870 [39][40][41][42] . Another, higher-resolution GWAS revealed the strongest association in the CCDC26 locus: rs55705857 with PBT [32,43] . A specific nucleotide in a CCDC26 SNP is a risk factor in low-grade (I-II) glioma, but not necessarily in high grade (III-IV) glioma cases [44] .…”

Section: Ccdc26 In Gliomamentioning

confidence: 99%

The role of the CCDC26 long noncoding RNA as a tumor suppressor

Hirano

2015

RNA Dis

View full text Add to dashboard Cite

CCDC26 on chromosome 8q24 is considered to encode a long intergenic noncoding RNA because the short open reading frame within the mRNA transcribed from this gene is not conserved in any other species. Genome-wide analysis has revealed association of CCDC26 with certain tumors, for instance low-level glioma. Moreover, moderate amplifications of the whole or part of the CCDC26 genetic locus have been observed in pediatric acute myeloid leukemia patients. The CCDC26 gene is amplified in the HL-60 acute myeloid leukemia cell line, in which double minute chromosomes-abnormal tiny chromosomes-harbor the CCDC26 gene. We examined the function of CCDC26 by gene knock-down (KD) using short hairpin RNAs in K562 human myeloid leukemia cells. In four stable KD clones, CCDC26 expression was suppressed to 1% of its normal level by transcriptional gene suppression, not post-transcriptional suppression. The growth rates of these KD clones were reduced compared with those of control cells in media containing high serum concentrations. In contrast, in media containing much lower serum concentrations, the KD clones exhibited significantly higher growth rates than controls, and increased survival after serum withdrawal. Enhanced expression of a receptor tyrosine kinase, KIT, was detected in the KD clones, and treatment with ISCK03, a KIT inhibitor, eliminated their increased survival in the absence of serum. Therefore, CCDC26 seems to control myeloid leukemia cell growth through regulation of KIT expression. These observations suggest that CCDC26 is a tumor-suppressive long noncoding RNA because it suppresses the KIT oncogene that supports survival of cancer cells in the stem cell state.

show abstract

“…Previous large number of studies revealed that several candidate risk genetic variants of genes may associate with glioma, including 5p15.33 (rs2736100, TERT), 8q24.21 (rs4295627, CCDC26), 9p21.3 (rs4977756, CDKN2A-CDKN2B), 11q23.3 (rs498872, PHLDB1), and 20q13.33 (rs6010620, RTEL1) ( Shete et al, 2009;Schoemaker et al, 2010;Safaeian et al, 2013). In addition, other studies also indicated that the rs6010620 polymorphism in regulator of telomere elongation helicase1 (RTEL1) gene was associated with the risk of glioma (Chen et al, 2011;Li et al, 2013a;Walsh et al, 2013 gene named rs6010620 which locate at intron 12. RTEL1 is a DNA helicase.…”

Section: Introductionmentioning

confidence: 98%

“…Glioma are the most common adults tumors of the central nervous system (CNS), accounting for a majority (80%) of glioblastoma (Dolecek et al, 2012;Walsh et al, 2013). Although with optimal treatment, glioma have high mortality and morbidity, and median survival is just about 12-15 months (Ahmed et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Associations between the rs6010620 Polymorphism in RTEL1 and Risk of Glioma: a Meta-analysis of 20,711 Participants

Xiang²,

Tang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

show abstract

Genetic variants in telomerase-related genes are associated with an older age at diagnosis in glioma patients: evidence for distinct pathways of gliomagenesis

Cited by 44 publications

References 27 publications

The RTEL1 rs6010620 Polymorphism and Glioma Risk: a Meta-analysis Based on 12 Case-control Studies

The RTEL1 rs6010620 Polymorphism and Glioma Risk: a Meta-analysis Based on 12 Case-control Studies

The role of the CCDC26 long noncoding RNA as a tumor suppressor

Associations between the rs6010620 Polymorphism in RTEL1 and Risk of Glioma: a Meta-analysis of 20,711 Participants

Contact Info

Product

Resources

About