Relationship between loss of heterozygosity at microsatellite loci and computerized nuclear morphometry in...

Loss of heterozygosity (LOH) at 4 microsatellite loci (chromosomes 8p23, 8q24, 13q14 and 17p13) and the nuclear morphometric data were analyzed in 28 tumors from 28 patients with hepatocellular carcinoma (HCC). LOH was detected in 63.2% of the tumors with marker D8S264 (chromosome 8p23), in 52.6% with marker D8S1801 (chromosome 8q24), in 25.0% with marker D13S328 (chromosome 13q14), and in 52.4% with marker D17S796 (chromosome 17p13). LOH on 17p13 was most frequent in tumors that had reached more advanced stages (p < 0.05). The frequencies of LOH on 17p13 were significantly higher in tumors with portal invasion of cancer cells or intrahepatic metastasis than those without (p < 0.05). Moreover, capsule infiltration of cancer cells or hepatitis B viral infection were more frequently detected in patients with LOH on 17p13 in their tumors. The mean nuclear area (MNA) and the standard deviation (SDNA) of tumors with LOH on 17p13 were significantly larger than those of the other sites (p < 0.01). No significant relationships were found between the LOH on 8p23, 8q24 or 13q14 of HCC and the clinicopathologic data, MNA or SDNA. Therefore, LOH on 17p13 of HCC correlates with the stage, portal invasion of cancer cells, intrahepatic metastasis, and nuclear morphometry. These findings suggest that the LOH on 17p13 is closely connected to the progression of HCC and that nuclear morphometry is useful as an indicator of genetic alterations in HCC.