Recent studies have demonstrated the power of deep re-sequencing of the whole 
genome or exome in understanding cancer genomes. However, targeted capture of 
selected genomic whole gene-body regions, rather than the whole exome, have 
several advantages: 1) the genes can be selected based on biology or a 
hypothesis; 2) mutations in promoter and intronic regions, which have important 
regulatory roles, can be investigated; and 3) less expensive than whole genome 
or whole exome sequencing. Therefore, we designed custom high-density 
oligonucleotide microarrays (NimbleGen Inc.) to capture approximately 1.7 Mb 
target regions comprising the genomic regions of 28 genes related to colorectal 
cancer including genes belonging to the WNT signaling pathway, as well as 
important transcription factors or colon-specific genes that are over expressed 
in colorectal cancer (CRC). The 1.7 Mb targeted regions were sequenced with a 
coverage ranged from 32× to 45× for the 28 genes. We identified a total of 2342 
sequence variations in the CRC and corresponding adjacent normal tissues. Among 
them, 738 were novel sequence variations based on comparisons with the SNP 
database (dbSNP135). We validated 56 of 66 SNPs in a separate cohort of 30 CRC 
tissues using Sequenom MassARRAY iPLEX Platform, suggesting a validation rate of 
at least 85% (56/66). We found 15 missense mutations among the exonic 
variations, 21 synonymous SNPs that were predicted to change the exonic splicing 
motifs, 31 UTR SNPs that were predicted to occur at the transcription factor 
binding sites, 20 intronic SNPs located near the splicing sites, 43 SNPs in 
conserved transcription factor binding sites and 32 in CpG islands. Finally, we 
determined that rs3106189, localized to the 5' UTR of antigen presenting tapasin 
binding protein (TAPBP), and rs1052918, localized to the 3' UTR of transcription 
factor 3 (TCF3), were associated with overall survival of CRC patients.