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Roles of reactive oxygen species in hepatocarcinogenesis and drug resistance gene expression in liver cancers
Author(s) -
Tien Kuo M.,
Savaraj Niramol
Publication year - 2006
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20240
Subject(s) - biology , reactive oxygen species , downregulation and upregulation , hepatocellular carcinoma , carcinogen , liver cancer , gene expression , cancer research , gene , drug resistance , cancer , drug , immunology , pharmacology , genetics
Hepatocellular carcinoma (HCC) has traditionally been an attractive system for cancer research because many animal HCC models are available. It is well known that liver tumors in animals can be induced by many different protocols, such as chronic hepatitis viral infections, carcinogens, toxins, steroid hormones, and dietary intervention. Although these different inducers have different cellular targets and modes of cytotoxic effects, their common denominator is the formation of reactive oxygen species (ROS). In this review, we present compelling evidence to support the hypothesis that ROS play important roles in hepatocarcinogenesis and the associated upregulation of drug resistance gene expression. © 2006 Wiley‐Liss, Inc.

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