Progression from colorectal adenoma to carcinoma is associated with non-random chromosomal gains as detected by comparative genomic hybridisation

Aims-Chromosomal gains and losses were surveyed by comparative genomic hybr idisation (CGH) in a series of colorectal adenomas and carcinomas, in searc h of high risk genomic changes involved in colorectal carcinogenesis. Methods-Nine colorectal adenomas and 14 carcinomas were analysed by CGH, an d DNA ploidy was assessed with both flow and image cytometry. Results-In the nine adenomas analysed, an average of 6.6 (range I to II) ch romosomal aberrations were identified. In the 14 carcinomas an average of 1 1.9 (range 5 to 17) events were found per tumour. In the adenomas the numbe r of gains and losses was in balance (3.6 v 3.0) while in carcinomas gains occurred more often than losses (8.2 v 3.7). Frequent gains involved 13q, 7 p, 7q, 8q, and 20q, whereas losses most often occurred at 18q, 4q, and 8p. Gains of 13q, 8q, and 20q, and loss of 18q occurred more often in carcinoma s than in adenomas (p = 0.005, p = 0.05, p = 0.05, and p = 0.02, respective ly). Aneuploid tumours showed more gains than losses (mean 9.3 v 4.9, p = 0 .02), in contrast to diploid tumours where gains and losses were nearly bal anced (mean 3.1 v 4.1, p = 0.5). Conclusion-The most striking difference between chromosomal aberrations in colorectal adenomas and carcinomas, as detected by CGH, is an increased num ber of chromosomal gains that show a nonrandom distribution. Gains of 13q a nd also of 20q and 8q seem especially to be involved in the progression of adenomas to carcinomas, possibly owing to low level overexpression of oncog enes at these loci.