Chromosomal alterations in ulcerative colitis-related and sporadic colorectal cancers by comparative genomic hybridization

Both ulcerative colitis (UC)-related and sporadic colorectal cancers are th ought to evolve through a multistep process of genomic instability accumula tion of genomic alterations, and clonal expansion. This process may involve different genomic changes in UC-related cancers than in sporadic cancers b ecause of the origin of UC-related cancers in an inflammatory field. This s tudy was designed to define the specific genomic events occurring in UC-rel ated cancers. Comparative genomic hybridization (CGH) was performed on 32 U C-related and 42 stage-matched sporadic colorectal cancers. The mean number of chromosomal alterations per case was similar in the UC-related and spor adic tumor groups (8.6 in UC, 8.1 in sporadic). The 2 tumor groups shared m any chromosomal alterations: losses on 18q (78% UC v 69% sporadic), 8p (53% v 50%), 17p (44% v 57%), and gains on 8q (63% v 45%), 20q (44% UC v 67%), and 13q (44% UC v 38%). However, differences in the frequency and timing of specific alterations were observed. Chromosome 5q was lost in 56% of UC-re lated but in only 26% of sporadic cancers. Alterations of chromosome 8 were associated with stage progression in UC-related, but not in sporadic cance rs. In contrast, 18q loss was associated with stage progression in sporadic cancers only. Thus, differences in the frequency and timing of individual chromosomal alterations suggest that genetic progression in these 2 tumor g roups may follow multiple pathways. HUM PATHOL 31:109-114. Copyright (C) 20 00 by W.B. Saunders Company.