To examine the relationship between the incidence of p53 gene deletion in each nucleus and the clinicopathological features in colorectal cancers, we performed a cytogenetic study using fluorescence in situ hybridization (FISH). FISH was performed on 5 adenomas and 38 colorectal cancers that had been resected surgically. The nucleus, in which the copy number of the p53 signal was lower than that of chromosome 17, was determined as a deletion of the p53 gene. The mean frequency of the deletion of p53 in adenomas and cancers were 7.8% +/- 3.0% and 57.0% +/- 19.0%, respectively. Numerical aberrations of chromosome 17 or a deletion of p53 were also detected in DNA diploidy. The mean frequency of the deletion of p53 in 32 cases with aneusomy of chromosome 17 (65.7% +/- 14.5%) was significantly higher than that in cases of disomy (51.1% +/- 19.3%, P < 0.05). Even though this frequency was high in the early stage, it was not associated with any specific histopathological features. This frequency was also higher in double primary cancers (70.4% +/- 16.7%) compared with single colorectal cancers (53.4% +/- 18.1%) (P < 0.05). Using FISH, our results demonstrated that the clonal deletion of the p53 locus is an early genetic event of colorectal cancers and that a high incidence of p53 deletion may influence the occurrence of double primary cancers.