BACKGROUND.
Numerical chromosome analysis has been established in solid tumors by using in situ hybridization ( 1 9 1 ) with a cliromosome-specific probe. We analy& human hepatocellular carcinoma [HCC) by I S 1 for chrornosonic 17 and investigated the correlation o f its copy number with histologic malignancy, proliferative activity, p53 mutation, and DNA ploidy.
METHODS.
Chromosome 17 was hybridized with a pericentroniere-specific 1)NA probe directly on the tumor cells isolated from paraffin blocks o f 25 surgically resected IlC(:s. Proliferative activity was measured by Ki-67 immunohistocliemistry. p5.7 mutation was analyzed by p53 inimunohistoclieniist~, and DKA ploidy was estimated by cytofluorometry.
RESULTS. 1:ortV-four percent of the 25 H(:Cs showed numerical abnormality of chromosome 17. Many disoinic cases had a less malignant histolohy, whereas many polysomic cases had a more malignant histology. The Ki-67 positive index of polysomic cases was higher than that of disomic cases. In 22 cases (88.0%). the copy number of chromosome 17 was well matched with DNA ploidy. tiowever, the numerical abnormality of chromosome 17 did not show a significant correlation with p53 mutation. Two of four HCCs that showed histologic heterogeneity were also heterogenous on ploidy pattern and the copy number of chromosome 17.
Conversely, there was one case in which only ISH could demonstrate hcterogeneity, although the other features exhibited homogeneity.