Among chromosome defects in colon cancer, deletions in 1p, 17p, and 18q have been reported as frequent events. To verify this, we investigated 1p, 17p, and 18q aneusomy in 60 colorectal cancers and their surrounding mucosa by means of fluorescence in situ hybridization (FISH). We also evaluated ERBB2 gene (alias HER-2/neu) amplification in a subset of tumors. The genetic picture in tumors was correlated with chromosomal alterations in normal colonic mucosae, as well with clinicopathologic variables. A population of cells in morphologically normal epithelium possesses genetic aberrations common to those in colon cancer, although in different percentages. No significant difference emerged in terms of fraction of nuclei with 17p monosomy between primary tumors and distal mucosal samples. Of tumor samples aneusomic for the three chromosomes, 58.3% also showed aneusomy in related normal colonic mucosa. In neoplastic samples, significant correlation existed between 1p aneusomy and mucosal component (P<0.007), between 17p aneusomy and increased depth of invasion (T3-T4) (P<0.05), and between 18q aneusomy and tumor site (P<0.03). None of the evaluated samples, neoplastic or normal, showed ERBB2 gene amplification.