To a better understanding for molecular mechanism of oncogenesis in hepatoma, primary hepatocellular carcinoma and hepatoma cell lines(Hep 3B, PLC/PRF/3, 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). Genes
of
AMY1A, CGA, SEA and HSTF1 were located on 1p21 and 6q14 respectively. SEA and HSTF1 were located on 11q13.
Regions of chromosome abnormalities in PLC/PRE/5 were the same found in Hep 3B. Besides, del(1q32) and del(1p32) were also cloned. Gene of CR1 and MYCL1 were located on 1q32 and 1p32 respectively. The characteristic findings of chromosome
abnormalities
in Hep G2 were del(1p31) and del(1q22). And GST1 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 AMY1A gene or near this gene
and
leads
to loss of functions to this gene. And impaired regulation of CGA occurs in next step. SEA, HSTF1 and MYCL1 oncogenes may act as a progressing factor of tumourgenesis in HBsAg(+) hepatoma. Some factors like chemical agents may cause functional
loss
of
GBT1 and DAF at first and functional loss of cell regulation of CGA occurs in next step. SKI oncogene may promote the progression of carcinogenesis 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.
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