表皮生长因子+61 G/A 与中国人种脑胶质瘤风险的相关性研究。
Association between EGF +61 G/A and glioma risk in a Chinese population.
机构信息
State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
出版信息
BMC Cancer. 2010 May 21;10:221. doi: 10.1186/1471-2407-10-221.
BACKGROUND
Epidermal growth factor (EGF) is critical in cancer process. EGF and EGF receptor (EGFR) interaction plays a pivotal role in cell proliferation, differentiation, and tumorigenesis of epithelial tissues. Variations of the EGF +61G/A (rs4444903) may lead to an alteration in EGF production and/or activity, which can result in individual susceptibility to brain glioma. The purpose of this study was to investigate the potential association between EGF +61G/A and brain glioma in a Chinese population.
METHODS
In this study, we analyzed single nucleotide polymorphism of EGF +61G/A in 677 patients with glioma and 698 gender- and age-matched controls. Genotyping was performed by polymerase chain reaction-ligation detection reaction (PCR-LDR) method.
RESULTS
The A allele (minor Allele) was 33.0% in cases and 27.3% in controls. The additive model was more powerful to reveal the association in our study than that of recessive and dominant model. Our data showed the genotype G/A and A/A was associated with increased risk for glioma (adjusted OR = 1.48, 95%CI: 1.17-1.87, p = 0.001 for G/A, adjusted OR = 1.81, 95%CI: 1.20-2.72, p = 0.005 for A/A, respectively), and for glioblastoma (adjusted OR = 1.51, 95%CI: 1.06-2.17, p = 0.024 and adjusted OR = 2.35, 95%CI: 1.34-4.15, p = 0.003, respectively). The A allele significantly increased glioma risk (OR = 1.31, 95%CI: 1.11-1.55, p = 0.001). The additive model (G/G vs G/A vs A/A) showed that both G/A and A/A genotype increased glioma risk (adjusted OR = 1.40, 95% CI: 1.17-1.66, p = 0.0002).G/A and A/A genotypes or EGF +61 A allele increased risk in both low and high WHO grade glioma. Non-smokers with G/A and A/A genotype showed increased glioma risk compared with G/G genotype (adjusted OR = 1.72, 95%CI: 1.29-2.30, p = 0.0002 and adjusted OR = 1.81, 95%CI: 1.10-2.99, p = 0.020, respectively). This association was not found in ever- or current-smokers.
CONCLUSIONS
Our study indicated that G/A and A/A genotypes or EGF +61 A allele were associated with higher glioma risk in Chinese. This is in contrast with previous studies which reported G allele as a risk factor of glioma in Caucasian. The role of EGF +61 A/G polymorphism in glioma susceptibility needs further investigation.
背景
表皮生长因子（EGF）在癌症进程中至关重要。EGF 和 EGF 受体（EGFR）的相互作用在上皮组织的细胞增殖、分化和肿瘤发生中起着关键作用。EGF+61G/A（rs4444903）的变异可能导致 EGF 产生和/或活性的改变，从而导致个体易患脑胶质瘤。本研究旨在探讨 EGF+61G/A 在中国人群中与脑胶质瘤的潜在关联。
方法
本研究分析了 677 例胶质瘤患者和 698 例性别和年龄匹配的对照者 EGF+61G/A 的单核苷酸多态性。采用聚合酶链反应-连接检测反应（PCR-LDR）法进行基因分型。
结果
病例组中的 A 等位基因（次要等位基因）为 33.0%，对照组为 27.3%。与隐性和显性模型相比，加性模型更能揭示我们研究中的关联。我们的数据表明，基因型 G/A 和 A/A 与胶质瘤风险增加相关（调整后的 OR=1.48，95%CI：1.17-1.87，p=0.001 用于 G/A，调整后的 OR=1.81，95%CI：1.20-2.72，p=0.005 用于 A/A），且与胶质母细胞瘤相关（调整后的 OR=1.51，95%CI：1.06-2.17，p=0.024 和调整后的 OR=2.35，95%CI：1.34-4.15，p=0.003）。A 等位基因显著增加了胶质瘤的风险（OR=1.31，95%CI：1.11-1.55，p=0.001）。加性模型（G/G 与 G/A 与 A/A）显示 G/A 和 A/A 基因型均增加了胶质瘤的风险（调整后的 OR=1.40，95%CI：1.17-1.66，p=0.0002）。G/A 和 A/A 基因型或 EGF+61A 等位基因增加了低和高世界卫生组织分级的胶质瘤风险。与 G/G 基因型相比，非吸烟者的 G/A 和 A/A 基因型显示出增加的胶质瘤风险（调整后的 OR=1.72，95%CI：1.29-2.30，p=0.0002 和调整后的 OR=1.81，95%CI：1.10-2.99，p=0.020）。在曾经吸烟者或当前吸烟者中未发现这种关联。
结论
我们的研究表明，G/A 和 A/A 基因型或 EGF+61A 等位基因与中国人群中较高的胶质瘤风险相关。这与之前报道的在白种人中 G 等位基因是胶质瘤风险因素的研究结果相反。EGF+61A/G 多态性在胶质瘤易感性中的作用需要进一步研究。
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