Associations between arachidonic acid metabolism gene polymorphisms and prostate cancer risk.
Associations between arachidonic acid metabolism gene polymorphisms and prostate cancer risk.
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DOI：
10.1002/pros.21354
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发表时间：
2011-09-15
期刊：
影响因子：
--
通讯作者：
Scheurer ME
中科院分区：
文献类型：
--
作者：
Amirian ES;Ittmann MM;Scheurer ME
花生四烯酸（AA）途径被怀疑参与各种癌症的发展，包括前列腺癌。然而，AA通路基因的单核苷酸多态性（SNPs）的作用仍然不清楚。本病例对照研究的目的是评估前列腺癌风险与PTGS 2、PTGES 2、ALOX 5、ALOX 5AP和LTA 4 H基因中14个此类SNP之间的关联。对585例白色前列腺癌病例和585例年龄匹配的健康对照者进行基因分型。每个SNP的最佳遗传模型使用Akaike的信息准则来确定。计算每个SNP与前列腺癌风险之间关联的比值比，包括总体和肥胖分层（BMI≥30）。对PTGES 2 SNP进行单倍型分析。LTA 4 H rs 1978331与前列腺癌总体风险呈负相关（TC vs TT/CC的超显性模型OR=0.68，95% CI：0.51-0.91）。在非肥胖个体中，PTGES 2 rs 10987883 GG基因型与前列腺癌风险增加相关（隐性模型OR=3.23，95%CI：1.27-8.23）。我们的研究结果表明，某些AA代谢基因的SNPS可能影响前列腺癌的易感性。此外，除了几种代谢后遗症外，肥胖还可能引起慢性低水平炎症状态，可能会改变这些SNP的影响。这些发现应该在更大规模的研究中得到证实，以检测肥胖的差异效应。看看这些影响是否因种族/民族而异也很有趣，特别是因为非洲裔美国人患前列腺癌的风险更高。
The arachidonic acid (AA) pathway is suspected to be involved in the development of various cancers, including prostate cancer. However, the role of single nucleotide polymorphisms (SNPs) of AA pathway genes remains unclear. The purpose of this case-control study was to evaluate the association between prostate cancer risk and 14 such SNPs in the PTGS2, PTGES2, ALOX5, ALOX5AP, and LTA4H genes. Genotyping was conducted on 585 white prostate cancer cases and 585 healthy, age-matched controls. The best genetic model for each SNP was determined using Akaike’s information criterion. Odds ratios for the association between each SNP and prostate cancer risk were calculated, both overall and stratified by obesity (BMI≥30). Haplotype analysis was conducted for the PTGES2 SNPs. LTA4H rs1978331 was inversely associated with prostate cancer risk overall (overdominant model OR=0.68, 95% CI: 0.51-0.91 for TC vs TT/CC). Among non-obese individuals, the GG genotype of PTGES2 rs10987883 was associated with an increased risk for prostate cancer (recessive model OR=3.23, 95% CI: 1.27-8.23). Our results indicate that SNPS in certain AA metabolism genes may influence prostate cancer susceptibility. Furthermore, it is possible that obesity, which induces a chronic state of low-level inflammation in addition to several metabolic sequelae, may modify the impact of these SNPs. These findings should be confirmed in a larger study with power to detect differential effects by obesity. It would also be interesting to see if these effects differed by racial/ethnic group, especially since African-American men are at higher risk of prostate cancer.
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影响因子：
3.5
作者：
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通讯作者：
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影响因子：
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作者：
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