Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-3-31
pubmed:abstractText
The aim of this study is to clarify the existence and the form of HCV RNA and HBV DNA genome integration and genetic instability in liver tissue with HBsAg-negative and anti-HCV-positive HCC. We investigated 16 Japanese patients with HBsAg-negative and anti-HCV-positive HCC. HBV genome integration into host cell genome by Southern hybridization and PCR was examined. Moreover, we analyzed loss of heterozygosity (LOH) and replication errors (RER) of chromosomes 2p, 3p and 17p using the PCR and an autosequencer to determine the three microsatellite regions D2S123, D3S1067, TP53. Eight (50.0%) of 16 were found to have integrated genome of HBV in tumor tissue (T) by PCR. In even the non-tumor regions (NT), seven patients (43.8%) were found to have HBV genome integration. The coincidence between T and NT was found in 4 (25%). Integration of HBV-X gene in T was revealed in three (18.7%), and HBV-integration was confirmed in all NT. No integration of the X gene alone was found in the liver tissue. Five (37.5%) of eight HBV DNA integrated cases simultaneously had HCV RNA minus strand. Concerning the genetic instability, RER were detected in two of 16 (12.5%). RER at 2p; D2S123 was observed in one of 16 (6.2%) and at 3p; D3S1067 was observed in one (6.2%). LOH at the D2S123 locus was observed in one of 12 tumors with heterozygosity (8.3%). There was no genetic instability (LOH or RER) of TP53 which was p53 locus on 17p in T. There was only one case of eight HBV DNA integrated cases (6.2%) with genetic instability of RER of 3p simultaneously in T. In conclusion, the majority of HBsAg-negative and anti-HCV-positive HCC liver tissue was found to have HCV-RNA and HBV DNA integration, and in some samples, HBV DNA integration and genetic instability were concurrently confirmed. It is speculated that multistep carcinogenesis may have been proposed for HCC oncogenetic progression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0304-3835
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
119
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-61
pubmed:meshHeading
pubmed-meshheading:18372522-Aged, pubmed-meshheading:18372522-Blotting, Southern, pubmed-meshheading:18372522-Carcinoma, Hepatocellular, pubmed-meshheading:18372522-DNA, Viral, pubmed-meshheading:18372522-Female, pubmed-meshheading:18372522-Hepacivirus, pubmed-meshheading:18372522-Hepatitis B, pubmed-meshheading:18372522-Hepatitis B Surface Antigens, pubmed-meshheading:18372522-Hepatitis B virus, pubmed-meshheading:18372522-Hepatitis C, pubmed-meshheading:18372522-Hepatitis C Antigens, pubmed-meshheading:18372522-Humans, pubmed-meshheading:18372522-Japan, pubmed-meshheading:18372522-Liver Neoplasms, pubmed-meshheading:18372522-Loss of Heterozygosity, pubmed-meshheading:18372522-Male, pubmed-meshheading:18372522-Middle Aged, pubmed-meshheading:18372522-RNA, Viral, pubmed-meshheading:18372522-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18372522-Virus Integration
pubmed:year
1997
pubmed:articleTitle
HBV genome integration and genetic instability in HBsAg-negative and anti-HCV-positive hepatocellular carcinoma in Japan.
pubmed:affiliation
Department of Medicine, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't