Chromosomal abnormality in hepatocellular carcinoma by comparative genomichybridisation in Taiwan

The elucidation of the genetic changes of hepatocellular carcinoma (HCC) is very important for understanding the molecular mechanism of liver carcinog enesis. In order to identify the gains or losses in DNA sequence copy numbe r in HCC, we used comparative genomic hybridisation to study 40 cases (44 t umours) of HCC. Tumour DNA and DNA from non-neoplastic liver tissue were la belled with different fluorochromes and then simultaneously hybridised to n ormal metaphase spread chromosomes. An image acquisition system was used to quantitate signal intensities contributed by tumour and reference DNA alon g the entire length of each chromosome. Regions of amplification and deleti on were demonstrated as quantitative alterations. Losses were prevalent on chromosome regions 16q (43%), 17p (20%), 13q (20%), 4q (15%) and 8p (15%). Gains frequently occurred on 8q (30%), 1q (20%), 6p (20%) and 17q (18%). He patitis B virus carriers had a significantly higher frequency of losses on chromosome 16q. Furthermore, the minimal region of losses was narrowed down to 16q11-q22. This study confirms the presence of previously known chromos omal aberrations in HCC and highlights a new significant correlation betwee n losses on chromosome 16q and hepatitis B virus carriers. (C) 1999 Elsevie r Science Ltd. All rights reserved.