Su H, Chang C, Hao J, et al. - Given the uncertainty concerning the molecular mechanism of perineural invasion (PNI) in stage II colorectal cancer (CRC), researchers here examined the genomic aberrations related to PNI in stage II CRC. They analyzed primary tumor tissues and paracancerous normal tissues of stage II CRC with and without PNI. In stage II CRC, the most frequent gains were noted at 7q11.21-q11.22, 8p11.21, 8p12-p11.23, 8q11.1-q11.22, 13q12.13-q12.2, and 20q11.21-q11.23 and the most frequent losses were noted at 17p13.1-p12, 8p23.2, and 118q11.2-q23. In Stage II CRC, they detected four high-level amplifications at 8p11.23-p11.22, 18q21.1, 19q11-q12, and 20q11.21-q13.32 and homozygous deletions at 20p12.1. Frequency plot comparison together with detailed genomic analysis revealed gains at 7q11.21-q22.1, 16p11.2, 17q23.3-q25.3, 19p13.3-p12, and 20p13-p11.1, and losses at 11q11-q12.1, 11p15.5-p15.1, 18p11.21, and 18q21.1-q23 were more common in patients with PNI. Patients without PNI more frequently had gains at 8q11.1-q24.3, 9q13-q34.3, and 13q12.3-q13.1, and losses at 8p23.3-p12, 17p13.3-p11.2, and 21q22.12. Further validation showed that the NPNI group vs the PNI group had significant up-regulation of the expression of FLT1, FBXW7, FGFR1, SLC20A2 and SERPINI1. Some genes enriched in specific pathways were identified in GO and pathway analysis. These genomic changes in the PNI of stage II CRC may aid in attaining insight into the mechanisms underlying PNI and assessing candidate biomarkers.