Chromosome 20 Aberrations at the Diploid-Aneuploid Transition in Sporadic Colorectal Cancer

DNA aneuploid sublines in sporadic colorectal cancers (CRCs) are quite frequent (about 85%) and likely the consequence of chromosomal instability and DNA copy number aberrations (CNAs). In order to gain insight into the mechanisms of the diploid-aneuploid transition in CRCs, we compared the CNA status in both diploid and aneuploid sublines. We used fresh/frozen material from 17 aneuploid CRCs, which was separated into 17 DNA diploid and 17 aneuploid sublines using enrichment of the epithelial component by multiparameter flow cytometry and sorting. CNA status of both sublines was obtained by array comparative genomic hybridization. The DNA diploid sublines from the aneuploid CRCs showed already CNAs, in particular, gains at 20p and 20q. The same aberrations were detected at increased frequencies in the corresponding DNA aneuploid sublines. Moreover, the very frequent gains/losses of chromosomes 4, 7, 8, 13, 15, and 18 in the DNA aneuploid sublines were absent or rare in the DNA diploid sublines from the same sporadic aneuploid CRCs. The comparison of the DNA diploid and aneuploid sublines from aneuploid CRCs suggests that 20p and 20q gains may play a role in the diploid-aneuploid transition. The 20q chromosomal arm appears of particular interest since it harbors several genes implicated in chromosomal instability. Fresh/frozen multiple superficial and intra-tumor tissue samples of 17 diploid and 17 matched aneuploid colorectal adenocarcinomas. Test samples are compared to an external pool of normal male/female reference DNA.