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Genomic changes frequently occur in cancer cells during tumorigenesis from normal cells. Using the Illumina Human NS-12 single-nucleotide polymorphism (SNP) chip to screen for gene copy number changes in primary hepatocellular carcinomas (HCCs), we initially detected amplification of 35 genes from four genomic regions (1q21–41, 6p21.2–24.1, 7p13 and 8q13–23). By integrated screening of these genes for both DNA copy number and gene expression in HCC and colorectal cancer, we selected  CENPF  (centromere protein F/mitosin),  GMNN  (geminin, DNA replication inhibitor),  CDK13  (cyclin-dependent kinase 13), and  FAM82B  (family with sequence similarity 82, member B) as common cancer genes. Each gene exhibited an amplification frequency of ∼30% (range, 20–50%) in primary HCC (n = 57) and colorectal cancer (n = 12), as well as in a panel of human cancer cell lines (n = 70). Clonogenic and invasion assays of NIH3T3 cells transfected with each of the four amplified genes showed that  CENPF ,  GMNN , and  CDK13  were highly oncogenic whereas  FAM82B  was not. Interestingly, the oncogenic activity of these genes (excluding  FAM82B ) was highly correlated with gene-copy numbers in tumor samples (correlation coefficient, r>0.423), indicating that amplifications of  CENPF ,  GMNN , and  CDK13  genes are tightly linked and coincident in tumors. Furthermore, we confirmed that  CDK13  gene copy number was significantly associated with clinical onset age in patients with HCC ( P =  0.0037). Taken together, our results suggest that coincidently amplified  CDK13 ,  GMNN , and  CENPF  genes can play a role as common cancer-driver genes in human cancers.

Frequent Amplification of CENPF, GMNN and CDK13 Genes in Hepatocellular Carcinomas