Recent high-throughput transcript discoveries have yielded a growing recognition 
of long intergenic non-coding RNAs (lincRNAs), a class of arbitrarily defined 
transcripts (>200 nt) that are primarily produced from the intergenic space. 
lincRNAs have been increasingly acknowledged for their expressional dynamics and 
likely functional associations with cancers. However, differential gene dosage 
of lincRNA genes between cancer genomes is less studied. By using the 
high-density Human Omni5-Quad BeadChips (Illumina), we investigated genomic copy 
number aberrations in a set of seven tumor-normal paired primary human mammary 
epithelial cells (HMECs) established from patients with invasive ductal 
carcinoma. This Beadchip platform includes a total of 2,435,915 SNP loci 
dispersed at an average interval of ~700 nt throughout the intergenic region of 
the human genome. We mapped annotated or putative lincRNA genes to a subset of 
332,539 SNP loci, which were included in our analysis for lincRNA-associated 
copy number variations (CNV). We have identified 122 lincRNAs, which were 
affected by somatic CNV with overlapped aberrations ranging from 0.14% to 100% 
in length. lincRNA-associated aberrations were detected predominantly with copy 
number losses and preferential clustering to the ends of chromosomes. 
Interestingly, lincRNA genes appear to be less susceptible to CNV in comparison 
to both protein-coding and intergenic regions (CNV affected segments in 
percentage: 1.8%, 37.5%, and 60.6%, respectively). In summary, our study 
established a novel approach utilizing high-resolution SNP array to identify 
lincRNA candidates, which could functionally link to tumorigenesis, and provide 
new strategies for the diagnosis and treatment of breast cancer.