Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Carcinogenesis. 2013 Apr;34(4):885-92. doi: 10.1093/carcin/bgs407. Epub 2013 Jan 4.
Genome-wide association studies (GWASs) have mainly focused on top significant single nucleotide polymorphisms (SNPs), most of which did not have clear biological functions but were just surrogates for unknown causal variants. Studying SNPs with modest association and putative functions in biologically plausible pathways has become one complementary approach to GWASs. To unravel the key roles of mitogen-activated protein kinase (MAPK) pathways in cutaneous melanoma (CM) risk, we re-evaluated the associations between 47 818 SNPs in 280 MAPK genes and CM risk using our published GWAS dataset with 1804 CM cases and 1026 controls. We initially found 105 SNPs with P ≤ 0.001, more than expected by chance, 26 of which were predicted to be putatively functional SNPs. The risk associations with 16 SNPs around DUSP14 (rs1051849) and a previous reported melanoma locus MAFF/PLA2G6 (proxy SNP rs4608623) were replicated in the GenoMEL dataset (P < 0.01) but failed in the Australian dataset. Meta-analysis showed that rs1051849 in the 3' untranslated regions of DUSP14 was associated with a reduced risk of melanoma (odds ratio = 0.89, 95% confidence interval: 0.82-0.96, P = 0.003, false discovery rate = 0.056). Further genotype-phenotype correlation analysis using the 90 HapMap lymphoblastoid cell lines from Caucasians showed significant correlations between two SNPs (rs1051849 and rs4608623) and messenger RNA expression levels of DUSP14 and MAFF (P = 0.025 and P = 0.010, respectively). Gene-based tests also revealed significant SNPs were over-represented in MAFF, PLA2G6, DUSP14 and other 16 genes. Our results suggest that functional SNPs in MAPK pathways may contribute to CM risk. Further studies are warranted to validate our findings.
全基因组关联研究(GWAS)主要集中在顶级显著的单核苷酸多态性(SNP)上,其中大多数没有明确的生物学功能,只是未知因果变异的替代物。研究具有适度关联和假定功能的 SNP 已成为 GWAS 的一种补充方法。为了揭示丝裂原活化蛋白激酶(MAPK)途径在皮肤黑色素瘤(CM)风险中的关键作用,我们使用已发表的包含 1804 例 CM 病例和 1026 例对照的 GWAS 数据集,重新评估了 280 个 MAPK 基因中的 47818 个 SNP 与 CM 风险之间的关联。我们最初发现了 105 个 P ≤ 0.001 的 SNP,超过了预期的偶然发现,其中 26 个被预测为假定的功能性 SNP。在 GenoMEL 数据集(P < 0.01)中,DUSP14 周围的 16 个 SNP 及其先前报道的黑色素瘤基因座 MAFF/PLA2G6(代理 SNP rs4608623)的风险关联得到了复制,但在澳大利亚数据集未得到复制。Meta 分析显示,DUSP14 3'非翻译区的 rs1051849 与黑色素瘤风险降低相关(比值比= 0.89,95%置信区间:0.82-0.96,P = 0.003,假发现率= 0.056)。使用来自高加索人的 90 个 HapMap 淋巴母细胞系进行的进一步基因型-表型相关性分析显示,两个 SNP(rs1051849 和 rs4608623)与 DUSP14 和 MAFF 的信使 RNA 表达水平之间存在显著相关性(P = 0.025 和 P = 0.010)。基于基因的测试还表明,MAFF、PLA2G6、DUSP14 和其他 16 个基因中的显著 SNP 过度表达。我们的结果表明,MAPK 途径中的功能性 SNP 可能导致 CM 风险增加。需要进一步的研究来验证我们的发现。