CORE
🇺🇦
make metadata, not war
Services
Services overview
Explore all CORE services
Access to raw data
API
Dataset
FastSync
Content discovery
Recommender
Discovery
OAI identifiers
OAI Resolver
Managing content
Dashboard
Bespoke contracts
Consultancy services
Support us
Support us
Membership
Sponsorship
Community governance
Advisory Board
Board of supporters
Research network
About
About us
Our mission
Team
Blog
FAQs
Contact us
Absence of mutation of the p73 gene localized at chromosome 1p36.3 in hepatocellular carcinoma
Authors
A Nakagawara
AG Knudson
+36 more
AJ Levine
B Bressac
B Vogelstein
CA Jost
D Simon
DA Vesey
F Henkler
H Nagai
H Tsuda
IC Hsu
J Amano
K Honda
KH Buetow
M Fujimori
M Kaghad
M Mihara
N Nishida
P Chomczynski
P Coursaget
RB Ray
RM Lunn
S Ichimiya
S Kajikawa
S Kress
S Sakiyama
SF Ding
SH Yeh
T Kuroki
T Möröy
T Teramoto
W Adachi
XW Wang
Y Kazachkov
Y Murakami
Y Nimura
Z Piao
Publication date
Publisher
Nature Publishing Group
Doi
Cite
View
on
PubMed
Abstract
Accumulating evidence has demonstrated that aberration of the p53 tumour-suppressor gene is one of the pivotal genetic events in hepatocellular carcinogenesis. Recent reports suggest that the product of hepatitis B virus (HBV) interacts with p53 and that the hepatitis C virus (HCV) core protein reduces p53 expression. A novel p73 gene, which is related to p53, has recently been identified and mapped to chromosome 1p36.3, which is a locus of multiple tumour-suppressor genes for many cancers, including hepatocellular carcinoma (HCC) and neuroblastoma. Here, we investigated mRNA expression, allelotype and mutation of p73 in 48 HCCs obtained from untreated patients. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that p73 mRNA was expressed ubiquitously at low levels in all the tumour tissues, as well as in the adjacent normal liver tissues. The frequency of p73 loss of heterozygosity was observed in 20% of HCCs, but PCR-single strand conformation polymorphism (SSCP) analysis showed no mutations in the 48 tumours except for three types of polymorphisms. These results suggest that p73 may play a role in hepatocellular carcinogenesis in a different manner from a Knudson two-hit model. The regulatory mechanism of interaction between p73 and hepatitis viruses remains to be determined. © 1999 Cancer Research Campaig
Similar works
Full text
Open in the Core reader
Download PDF
Available Versions
Crossref
See this paper in CORE
Go to the repository landing page
Download from data provider
Last time updated on 03/01/2020