人类白细胞抗原 I 类等位基因与慢性髓性白血病风险的关系:一项荟萃分析。

Human leukocyte antigen class I alleles and the risk of chronic myelogenous leukemia: a meta-analysis.

机构信息

Department of Laboratory Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.

出版信息

Leuk Lymphoma. 2010 Jul;51(7):1288-92. doi: 10.3109/10428191003802340.

Abstract

A number of different human leukocyte antigen (HLA) allele associations with chronic myelogenous leukemia (CML) have been previously reported. The specific associations reported in one population, however, are rarely replicated in other populations. We attempted to explore these associations by performing a meta-analysis of published studies. Following a Medline search, we identified four studies which presented raw data on all allele associations with CML (significant and non-significant). Meta-analysis of these revealed a significant risk association with the HLA-A02 (pooled odds ratio 1.33, 95% confidence interval 1.10-1.61) allele and a significant protective effect with the HLA-B35 allele (pooled odds ratio 0.64, 95% confidence interval 0.48-0.86). To our knowledge this is the first study to demonstrate the epidemiologic association between HLA-A*02 and the risk of CML, and we discuss this in the context of recent immunological studies reporting data on BCR-ABL fusion peptide presentation and subsequent immune response. Our findings suggest that individual epidemiological studies may lack statistical power, or may have other interfering factors which prevent the unmasking of overall associations. Meta-analyses of published studies may overcome these limitations and may prove useful in uncovering allele-disease associations.

摘要

先前已有多项研究报告指出,多种人类白细胞抗原(HLA)等位基因与慢性髓细胞白血病(CML)有关。然而,在一个人群中报告的特定关联很少在其他人群中得到复制。我们试图通过对已发表的研究进行荟萃分析来探讨这些关联。通过 Medline 搜索,我们确定了四项提供与 CML 所有等位基因关联的原始数据(有意义和无意义)的研究。对这些研究进行荟萃分析显示,HLA-A02 等位基因与 CML 风险呈显著相关(合并优势比 1.33,95%置信区间 1.10-1.61),而 HLA-B35 等位基因则具有显著的保护作用(合并优势比 0.64,95%置信区间 0.48-0.86)。据我们所知,这是第一项证明 HLA-A*02 与 CML 风险之间存在流行病学关联的研究,我们结合最近报告 BCR-ABL 融合肽呈递和随后免疫反应数据的免疫研究对此进行了讨论。我们的研究结果表明,个别流行病学研究可能缺乏统计学效力,或者可能存在其他干扰因素,从而无法揭示总体关联。已发表研究的荟萃分析可能会克服这些局限性,并可能有助于揭示等位基因与疾病的关联。

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