Genome-wide association studies have identified more than 70 common variants 
that are associated with breast cancer risk. Most of these variants map to 
non-protein-coding regions and several map to gene deserts, regions of several 
hundred kilobases lacking protein-coding genes. We hypothesized that gene 
deserts harbor long-range regulatory elements that can physically interact with 
target genes to influence their expression. To test this, we developed Capture 
Hi-C (CHi-C), which, by incorporating a sequence capture step into a Hi-C 
protocol, allows high-resolution analysis of targeted regions of the genome. We 
used CHi-C to investigate long-range interactions at three breast cancer gene 
deserts mapping to 2q35, 8q24.21, and 9q31.2. We identified interaction peaks 
between putative regulatory elements ("bait fragments") within the captured 
regions and "targets" that included both protein-coding genes and long noncoding 
(lnc) RNAs over distances of 6.6 kb to 2.6 Mb. Target protein-coding genes were 
IGFBP5, KLF4, NSMCE2, and MYC; and target lncRNAs included DIRC3, PVT1, and 
CCDC26. For one gene desert, we were able to define two SNPs (rs12613955 and 
rs4442975) that were highly correlated with the published risk variant and that 
mapped within the bait end of an interaction peak. In vivo ChIP-qPCR data show 
that one of these, rs4442975, affects the binding of FOXA1 and implicate this 
SNP as a putative functional variant.