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首页> 外文期刊>Cancer epidemiology, biomarkers and prevention: A publication of the American Association for Cancer Research >Polymorphisms in apoptosis and cell cycle control genes and risk of brain tumors in adults.
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Polymorphisms in apoptosis and cell cycle control genes and risk of brain tumors in adults.

机译:成人细胞凋亡和细胞周期控制基因多态性与脑肿瘤的风险。

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摘要

Despite the potential importance of the cell cycle and apoptosis pathways in brain tumor etiology, little has been published regarding brain tumor risk associated with common gene variants in these pathways. Using data from a hospital-based case-control study conducted by the National Cancer Institute between 1994 and 1998, we evaluated risk of glioma (n = 388), meningioma (n = 162), and acoustic neuroma (n = 73) with respect to 12 single nucleotide polymorphisms from 10 genes involved in apoptosis and cell cycle control: CASP8, CCND1, CCNH, CDKN1A, CDKN2A, CHEK1, CHEK2, MDM2, PTEN, and TP53. We observed significantly decreased risk of meningioma with the CASP8 Ex14-271A>T variant [odds ratio (OR)(AT), 0.8; 95% confidence interval (95% CI), 0.5-1.2; OR(AA), 0.5; 95% CI, 0.3-0.9; P(trend) = 0.03] and increased risk of meningioma with the CASP8 Ex13+51G>C variant (OR(GC), 1.4; 95% CI, 0.9-2.1; OR(CC), 3.6; 95% CI, 1.0-13.1; P(trend) = 0.04). The CT haplotype of the two CASP8 polymorphisms was associated with significantly increased risk of meningioma (OR, 1.7; 95% CI, 1.1-2.6), but was not associated with risk of glioma or acoustic neuroma. The CCND1 Ex4-1G>A variant was associated with increased risk for glioma, and the Ex8+49T>C variant of CCNH was associated with increased risk of glioma and acoustic neuroma. The MDM2 Ex12+162A>G variant was associated with significantly reduced risk of glioma. Our results suggest that common variants in the CASP8, CCND1, CCNH, and MDM2 genes may influence brain tumor risk. Future research in this area should include more detailed coverage of genes in the apoptosis/cell cycle control pathways.
机译:尽管细胞周期和细胞凋亡途径在脑肿瘤病因学中具有潜在的重要性,但关于与这些途径中常见基因变异相关的脑肿瘤风险的报道很少。使用美国国家癌症研究所(National Cancer Institute)在1994年至1998年间进行的一项基于医院的病例对照研究的数据,我们评估了神经胶质瘤(n = 388),脑膜瘤(n = 162)和听神经瘤(n = 73)的风险至10个参与凋亡和细胞周期控制的基因的12个单核苷酸多态性:CASP8,CCND1,CCNH,CDKN1A,CDKN2A,CHEK1,CHEK2,MDM2,PTEN和TP53。我们观察到CASP8 Ex14-271A> T变异株的脑膜瘤风险显着降低[几率(OR)(AT)为0.8; 95%置信区间(95%CI),0.5-1.2; OR(AA),0.5; 95%CI,0.3-0.9; P(趋势)= 0.03]和使用CASP8 Ex13 + 51G> C变体的脑膜瘤风险增加(OR(GC),1.4; 95%CI,0.9-2.1; OR(CC),3.6; 95%CI,1.0- 13.1; P(趋势)= 0.04)。两种CASP8基因多态性的CT单倍型与脑膜瘤风险显着增加有关(OR,1.7; 95%CI,1.1-2.6),但与神经胶质瘤或听神经瘤的风险无关。 CCND1 Ex4-1G> A变体与神经胶质瘤的风险增加有关,而CCNH的Ex8 + 49T> C变体与神经胶质瘤和听神经瘤的风险增加有关。 MDM2 Ex12 + 162A> G变体与胶质瘤的风险显着降低有关。我们的结果表明,CASP8,CCND1,CCNH和MDM2基因中的常见变异可能会影响脑瘤风险。该领域的未来研究应包括细胞凋亡/细胞周期控制途径中基因的更详细的报道。

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