The role of previous infection of hepatitis B virus in HBs antigen negative and anti-HCV negative Japanese patients with hepatocellular carcinoma: Etiological and molecular biological study (vol 18, pg 397, 1999)

Citation
Y. Matsuzaki et al., The role of previous infection of hepatitis B virus in HBs antigen negative and anti-HCV negative Japanese patients with hepatocellular carcinoma: Etiological and molecular biological study (vol 18, pg 397, 1999), J EXP CL C, 19(1), 2000, pp. 125-125
Citations number
1
Categorie Soggetti
Oncology
Journal title
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
ISSN journal
03929078 → ACNP
Volume
19
Issue
1
Year of publication
2000
Pages
125 - 125
Database
ISI
SICI code
0392-9078(200003)19:1<125:TROPIO>2.0.ZU;2-K
Abstract
The aim of this study is to elucidate the important role of the previous in fection of HBV, and the relations among HBV genome integration,p53 gene mut ation, telomerase activity and genetic instability in liver tissue with HBs Ag- negative(NB) and anti-HCV negative(NC) hepatocellular carcinoma (HCC). We examined the backgrounds of 34 NE and NC (NBNC) Japanese patients with c hronic liver disease (CLD) patients not associated with HCC and 26 NBNC CLD patients with HCC. HBV genome integration into host cell genome, p53 gene mutation, telomerase activity and genetic instability were examined in 6 wi th NBNC HCC (NBNC-HCC) tumorous tissue (T) and non tumorous tissues (NT). I n the NBNC group, HBV-related antibody positive patients with HCC are signi ficantly more than the patients without HCC. Moreover, concerning the stage of the coexisted liver diseases, in NBNC CLD, LC patients with HCC is 19 o f 26 (73.1%), on the other hand, LC patients without HCC is 16 of 34 (47.1% ). LC patients with HCC group is significantly more than that without HCC. Three (50%) of 6 in T and 3 cases (50%) in NT were found to integrated geno me of HBV. p53 gene mutation was observed in 3(50%) of T. Concerning the te lomerase activity, 3 of 6 cases (50%) in T and 1 case in NT was recognized. There was no genetic instability (LOH or RER) of D2S123, D3S1067 and TP53 in T and NT. Finally, in T of NBNC HCC cases, TTVDNA was detected in 3 of 5 . Even in the HBsAg-negative and anti-HCV negative HCC cases, CLD coexistin g with LC, previous HBV infection and HBVDNA integration were observed. The re were a few cases with HBVDNA integration, p53 gene mutation, telomerase activity and genetic instability, simultaneously in HCC tissue, and in some cases, the coexistence with TTVDNA were concurrently confirmed. It is spec ulated that the important role of the previous infection of HBV may have al so been proposed for HCC oncogentic progression in NBNC CLD.