Cytogenetic analysis of short-term cultures from colorectal adenomas revealed acquired clonal chromosome aberrations in I 4 of 17 tumors. In 4 adenomas, only numerical changes were found, whereas 10 had structural rearrangements. Trisomy 7 was found as the sole change in one of the tumors and together with other numerical changes in another. A + 7 was also present in one case with structural aberrations. Other recurrent numerical aberrations were -14 and -18, both found in 2 adenomas with structural karyotypic changes; in addition, one chromosome I 4 was lost in one of the tumors with only numerical changes. The chromosome most often involved in structural aberrations was chromosome I. In 6 cases, the rearrangements led t o changes in I p, always with loss of material. The breakpoints were at I p32-36. One adenoma had deletion of I p as the only change. Other chromosomes that were involved in changes in more than 2 cases were chromosomes 8, 13, and 17. These rearrangements typically led t o gain of 8q and I 3q and loss of I7p. The adenomas with structural abnormalities were generally larger and had a higher degree of dysplasia than did the adenomas with numerical changes only or those with a normal karyotype. All adenomas with a tubulovillous or villous architecture had structural rearrangements. Our findings confirm that a subset of colorectal adenomas exists that have only numerical chromosome aberrations. They also support our previous conclusion that loss of material from distal I p is an early event in colorectal tumorigenesis. but that other cytogenetic aberrations follow and typically are present already at the adenomatous stage. The accumulation of chromosome-level mutational events in adenomas correlates with the pathologic features: the more malignancy-like the phenotype, the more complex the karyotype. There seems t o be no single aberration that distinguishes colorectal adenomas from carcinomas, however. Genes Chromosom Cancer 10: 190-1 96 ( 1 994).