B형 간염 virus 양성 간암과 음성 간암의 세표유전학적 차이 = Cytogenetic differences between hepatitis B posotive and negative in hepatoma

다국어 초록 (Multilingual Abstract)

To a better understanding for molecular mechanism of oncogenesis in hepatoma, primary hepatocellular carcinoma and hepatoma cell lines(Hep 3B, PLC/PRF/5, Hep G2) were subjected to detailed cytogenetic analysis with G-banding method after cell cultures. No cloned chromosomal abnormalities were found in the primary hepatoma(below 10%). On the other hand, all hepatoma cell lines were cloned, the specific chromosomal abnormalities in Hep 3B were del(1p21), del(6q14) and t(1 : 11) (p11 : q13). Gen of AMYLA, CGA, SEA and HSTFl were located on 1p21 and 6q14 respectively. SEA and HSTFl were located on 11q13.
Regions of chromosome abnormalities in PLC / PRF / 5 were the same found in Hep 3B. Besides, del(1q32) and del(1p32) were also cloned. Gene of CRl and MYCLl were located on 1q32 and 1p32 respectively. The characteristic findings of chromosome abnormalities in Hep G2 were del(1p31) and del (1q22). And GSTl and DAF were located on these regions each other. Del(6q11) and del(1p22) were
also found in Hep G2. From the above results, it is presumed that HBV may integrate to AMYlA gene or near this gene and leads to ioss of functions to this gene. And impaired regulation of CGA occurs in next step. SEA, HSTFl and MYCLl oncogenes may act as a progressing factor of tumourgenesis in HBsAg(＋) hepatoma, Some factors like chemical agents may cause functional loss of GSTl and DAF at first and functional loss of cell regulation of CGA occurs in next step. SKI oncogene may promote the progression of carinogenesis in this cell line. Whether any causative agents are involed in carcinogenesis of hepatoma, fuctional loss of CGA gene is the most important factor in tumour-genesis
in hepatoma.