Cytogenetic aberrations detected by flow cytometry and fluorescence in situ hybridization in colorectal cancers: Two cytogenetic pathways in colorectal carcinogenesis

We measured DNA content by flow cytometry and determined the number of chro mosomes 7, 17 and 18 by fluorescence in situ hybridization using DNA probes in 38 sporadic colorectal adenocarcinomas including 14 early cancers. Base d on DNA ploidy and the copy number of chromosome 18, colorectal cancers we re divided into two groups. In early cancers (mucosal and submucosal adenoc arcinomas), monosomy 18 with DNA hypotriploidy was detected exclusively in 6 sessile tumors without adenoma portions. Seven of the remaining 8 tumors in which adenoma portions coexisted manifested disomy 18 and DNA diploidy o r near diploidy. These tumors were considered to occur along the adenoma-ca rcinoma sequence. In contrast, monosomy 18 was accompanied by DNA diploidy or near diploidy in advanced cancers penetrating the muscularis propria. In advanced cancers, DNA hypertriploidy was linked with disomy 18 and chromos omes 7 and 17 were trisomic or tetrasomic. Observations indicate at least t wo different cytogenetic pathways in colorectal carcinogenesis. According t o these findings, two thirds of advanced cancers were estimated to originat e from adenoma, and the others were not.