Camp Nicola J, Lin Wei-Yu, Bigelow Alex, Burghel George J, Mosbruger Timothy L, Parry Marina A, Waller Rosalie G, Rigas Sushilaben H, Tai Pei-Yi, Berrett Kristofer, Rajamanickam Venkatesh, Cosby Rachel, Brock Ian W, Jones Brandt, Connley Dan, Sargent Robert, Wang Guoying, Factor Rachel E, Bernard Philip S, Cannon-Albright Lisa, Knight Stacey, Abo Ryan, Werner Theresa L, Reed Malcolm W R, Gertz Jason, Cox Angela
University of Utah School of Medicine, Salt Lake City, Utah.
Department of Oncology and Metabolism, University of Sheffield, Sheffield, United Kingdom.
Cancer Res. 2016 Apr 1;76(7):1916-25. doi: 10.1158/0008-5472.CAN-15-1629. Epub 2016 Jan 21.
The findings from genome-wide association studies hold enormous potential for novel insight into disease mechanisms. A major challenge in the field is to map these low-risk association signals to their underlying functional sequence variants (FSV). Simple sequence study designs are insufficient, as the vast numbers of statistically comparable variants and a limited knowledge of noncoding regulatory elements complicate prioritization. Furthermore, large sample sizes are typically required for adequate power to identify the initial association signals. One important question is whether similar sample sizes need to be sequenced to identify the FSVs. Here, we present a proof-of-principle example of an extreme discordant design to map FSVs within the 2q33 low-risk breast cancer locus. Our approach employed DNA sequencing of a small number of discordant haplotypes to efficiently identify candidate FSVs. Our results were consistent with those from a 2,000-fold larger, traditional imputation-based fine-mapping study. To prioritize further, we used expression-quantitative trait locus analysis of RNA sequencing from breast tissues, gene regulation annotations from the ENCODE consortium, and functional assays for differential enhancer activities. Notably, we implicate three regulatory variants at 2q33 that target CASP8 (rs3769823, rs3769821 in CASP8, and rs10197246 in ALS2CR12) as functionally relevant. We conclude that nested discordant haplotype sequencing is a promising approach to aid mapping of low-risk association loci. The ability to include more efficient sequencing designs into mapping efforts presents an opportunity for the field to capitalize on the potential of association loci and accelerate translation of association signals to their underlying FSVs. Cancer Res; 76(7); 1916-25. ©2016 AACR.
全基因组关联研究的结果为深入了解疾病机制提供了巨大潜力。该领域的一个主要挑战是将这些低风险关联信号映射到其潜在的功能序列变异(FSV)。简单的序列研究设计并不充分,因为大量具有统计学可比性的变异以及对非编码调控元件的有限了解使优先级排序变得复杂。此外,通常需要大样本量才能有足够的能力识别初始关联信号。一个重要问题是,是否需要对类似的样本量进行测序以识别FSV。在此,我们展示了一个极端不一致设计的原理验证示例,用于在2q33低风险乳腺癌基因座内映射FSV。我们的方法采用对少量不一致单倍型进行DNA测序,以有效识别候选FSV。我们的结果与一项样本量比我们大2000倍的传统基于归因的精细定位研究结果一致。为了进一步确定优先级,我们使用了来自乳腺组织RNA测序的表达数量性状基因座分析、ENCODE联盟的基因调控注释以及差异增强子活性的功能测定。值得注意的是,我们发现2q33处的三个调控变异(CASP8中的rs376982�、rs3769821以及ALS2CR12中的rs10197246)具有功能相关性。我们得出结论,嵌套不一致单倍型测序是辅助映射低风险关联基因座的一种有前景的方法。将更高效的测序设计纳入映射工作的能力为该领域利用关联基因座的潜力并加速将关联信号转化为其潜在FSV提供了机会。《癌症研究》;76(7);1916 - 25。©2016美国癌症研究协会。