Investigation of Established Genetic Risk Variants for Glioma in Prediagnostic Samples from a Population-Based Nested Case–Control Study

Wibom, Carl; Späth, Florentin; Dahlin, Anna M.; Langseth, Hilde; Hovig, Eivind; Rajaraman, Preetha; Johannesen, Tom Børge; Andersson, Ulrika; Melin, Beatrice

doi:10.1158/1055-9965.epi-14-1106

Cited by 18 publications

(16 citation statements)

References 31 publications

(45 reference statements)

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“…A total of 6 publications including 16 case-control studies met the inclusion criteria (8,(10)(11)(12)(13)(14). The study selection process is outlined in Fig.…”

Section: Study Characteristicsmentioning

confidence: 99%

“…In recent years, several genes have been identified as potential glioma susceptibility genes, including RAD51, TP53, telomerase reverse transcriptase and regulator of telomere elongation helicase 1 (3)(4)(5)(6)(7)(8). Another important gene is coiled-coil domain-containing 26 (CCDC26), which increases the apoptosis of glioblastoma cells by modulating differentiation and apoptosis following induction by retinoic acid treatment (9).…”

Section: Introductionmentioning

confidence: 99%

“…The rs4295627 polymorphism is located in intron 3 of the CCDC26 gene. The G→A change in this single-nucleotide polymorphism (SNP) has been reported by several studies to affect CCDC26 expression and glioma risk (8,(10)(11)(12)(13)(14). However, the results were inconclusive, partially due to the possible small effect of the polymorphism on glioma risk and the relatively small sample size in each of published studies.…”

Section: Introductionmentioning

confidence: 99%

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Association of the CCDC26 rs4295627 polymorphism with the risk of glioma: Evidence from 7,290 cases and 11,630 controls

Wang

Luo

Ruan

et al. 2016

Molecular and Clinical Oncology

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Abstract. Published data on the association between the coiled-coil domain-containing 26 (CCDC26) rs4295627 polymorphism and the risk of glioma have been inconclusive. To further investigate this association, a meta-analysis was performed. By a comprehensive literature search using PubMed and EMBASE databases, a total of 16 case-control studies were identified for inclusion in the meta-analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess this association. Our results confirmed that the risk with allele G was higher compared with that with allele T for glioma. The results indicated that the allele G of rs4295627 polymorphism in the CCDC26 gene was associated with increased risk of glioma in the homozygote model (GG vs. TT, OR=1.936, 95 %CI: 1.500-2.658, P<0.001), the heterozygote model (GT vs. TT, OR=1.323, 95% CI: 1.241-1.412, P=0.206), the dominant model (GG+GT vs. TT, OR=1.375, 95% CI: 1.256-1.505, P=0.026), the recessive model (GG vs. GT+TT, OR=1.769, P<0.001) and the allele model (G vs. T, OR=1.310, 95% CI: 1.185-1.448, P<0.001). Current evidence suggests that the rs4295627 polymorphism in the CCDC26 gene may contribute to glioma susceptibility. However, further case-control studies are required to confirm our results.

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“…A total of 6 publications including 16 case-control studies met the inclusion criteria (8,(10)(11)(12)(13)(14). The study selection process is outlined in Fig.…”

Section: Study Characteristicsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association of the CCDC26 rs4295627 polymorphism with the risk of glioma: Evidence from 7,290 cases and 11,630 controls

Wang

Luo

Ruan

et al. 2016

Molecular and Clinical Oncology

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“…The main cause of poor prognosis is that glioma is characterized by rapid growth, high invasiveness and suppression of cell apoptosis (8,9). Besides, poorly understanding the etiology and progression of glioma hampers the development of treatments and surveillance strategies (10). Therefore, fully understanding the molecular mechanisms underlying occurrence, development and evolution of glioma is urgently needed to investigate novel and effective therapeutic treatments.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-302a targets GAB2 to suppress cell proliferation, migration and invasion of glioma

Jia

Liu

et al. 2016

Oncology Reports

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Glioma is the most frequent and aggressive primary tumor of the brain in humans. Over the last few decades, significant progress has been made in early detection and multi-mode treatments, but the prognosis of gliomas is still extremely poor. MicroRNAs are endogenously expressed non-coding, single strand and short RNA molecules. Increasing number of studies demonstrated that microRNAs are dysregulated in a variety of human cancers, and play significant roles in tumorigenesis and tumor development, including glioma. In the present study, we for the first time found that microRNA-302a (miR-302a) was significantly downregulated in both glioma tissues and cell lines. In glioma patients, low miR-302a expression was correlated with KPS score and WHO grade. Restoration of miR-302a expression inhibited cell proliferation, migration and invasion of glioma in vitro. In addition, GAB2 was identified as a direct target of miR-320a. In clinical glioma tissues, GAB2 was upregulated and in-versely correlated with miR-302a expression. GAB2 underexpression had similar biological roles with miR-302a overexpression in glio-ma cells, further confirming that GAB2 was a functional downstream target of miR-302a. Moreover, rescue experiments showed that upregulation of GAB2 effectively reversed the inhibition effects of miR-302a on glioma cells proliferation, migration and invasion. These findings suggested that miR-302a is an important tumor suppressor of glioma progression by directly targeting GAB2, thus providing new insight into the molecular mechanisms underlying glioma occurrence, development and evolution of glioma.

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“…Environmental risk factor for glioma is exposure to moderate to high doses of ionizing radiation and etiology of glioma genetic component contains an elevated glioma risk among individuals with a family history of glioma. The advanced understanding of aetiology of glioma has potential to facilitate treatment development, and thereby to improve the outcome of the disease [2]. The pathogenesis glioma remains largely unknown [3].…”

Section: Introductionmentioning

confidence: 99%

Screening of Glioma Patients for 1p/19q Region with Fluorescent Probes

Goud¹,

Matam²,

Vempati³

et al. 2016

MOJI

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Oligodendroglial tumors represent approximately 4-7% of all gliomas. The discovery of 1p and 19q chromosomal arms deletion in glial tumour influence the diagnosis and more accurate prediction of chemotherapy response. As a result, an attempt has been made to detect deletion using fluorescent insitu hybridization (FISH) and to determine its prognostic value in a cohort of glial tumour patients from Hyderabad population.

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Investigation of Established Genetic Risk Variants for Glioma in Prediagnostic Samples from a Population-Based Nested Case–Control Study

Cited by 18 publications

References 31 publications

Association of the CCDC26 rs4295627 polymorphism with the risk of glioma: Evidence from 7,290 cases and 11,630 controls

Association of the CCDC26 rs4295627 polymorphism with the risk of glioma: Evidence from 7,290 cases and 11,630 controls

MicroRNA-302a targets GAB2 to suppress cell proliferation, migration and invasion of glioma

Screening of Glioma Patients for 1p/19q Region with Fluorescent Probes

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