Loss of heterozygosity and microsatellite instability in hepatocellular carcinoma in Taiwan

Elucidation of the basic genetic changes of human hepatocellular carcinoma is important for the understanding and treatment of this cancer. We used mi crosatellite polymorphism markers to study 30 cases of hepatocellular carci noma (34 tumours) on all human chromosomes. DNA from 34 pairs of hepatocell ular carcinomas and corresponding non-tumour parts was prepared. Loss of he terozygosity (LOH) and microsatellite instability on 23 chromosomes were in vestigated by 231 sets of microsatellite markers. More than 20% LOH was sho wn for loci on 16q (47.1%), 13q (32.4%), 17p (32.4%), 50 (26.5%), 11p (23.5 %) and 9p (20.6%). the commonly affected regions were mapped to 16q12.1, 16 q12.2, 16q24, 13q12.1-32, 17p13, 5q32, 5q34, 5q3, 11p15, 11q23-24 and 9p21. Hepatitis B virus carriers had a significantly higher frequency of LOH on chromosomes 5q, 11p and 16q. Furthermore, larger tumour size tended to have higher frequency of LOH at D16S409 locus (16q12.1). Microsatellite instabi lity was only found in 12 of 231 markers and the frequency is very low. The se data suggest that the chromosomes 16q, 13q, 17p, 5q, 11p and 9p might pa rticipate in hepatocarcinogenesis. However, microsatellite instability migh t play little role in the development of this cancer in Taiwan.