ArticleProceedings of the National Academy of Sciences of the United States of America1993
Trans-activation of glutathione transferase P gene during chemical hepatocarcinogenesis of the rat.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 65 citations in OpenAlex.
- Review
- Oral administration of fructose exacerbates liver fibrosis and hepatocarcinogenesis via increased intestinal permeability in a rat steatohepatitis model.Oncotarget · 2018Article
- Metformin inhibits early stage diethylnitrosamine‑induced hepatocarcinogenesis in rats.Molecular medicine reports · 2016Article
- Dietary fructose enhances the incidence of precancerous hepatocytes induced by administration of diethylnitrosamine in rat.European journal of medical research · 2013Article
- Cancer chemopreventive potential of volatile oil from black cumin seeds, Nigella sativa L., in a rat multi-organ carcinogenesis bioassay.Oncology letters · 2010Article
- Development of glutathione S-transferase-P-negative foci accompanying nuclear factor-erythroid 2-related factor 2 expression during early stage of rat hepatocarcinogenesis.Cancer science · 2008Article
- Histone acetyltransferase MOZ acts as a co-activator of Nrf2-MafK and induces tumour marker gene expression during hepatocarcinogenesis.The Biochemical journal · 2007Article
- Mechanisms of a tumor marker, glutathione transferase P, expression during hepatocarcinogenesis of the rat.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2006Review
- Transcription factor Nrf2/MafK regulates rat placental glutathione S-transferase gene during hepatocarcinogenesis.The Biochemical journal · 2004Article
- Protection against diethylnitrosoamine-induced hepatocarcinogenesis by an indigenous medicine comprised of Nigella sativa, Hemidesmus indicus and Smilax glabra: a preliminary study.Journal of carcinogenesis · 2003Article
- Activation of mouse Pi-class glutathione S-transferase gene by Nrf2(NF-E2-related factor 2) and androgen.The Biochemical journal · 2002Article
- Inhibition of early-phase exogenous and endogenous liver carcinogenesis in transgenic rats harboring a rat glutathione S-transferase placental form gene.Japanese journal of cancer research : Gann · 1998Article
- Expression of glutathione S-transferase placental mRNA in hepatic preneoplastic lesions in rats.World journal of gastroenterology · 1998Article
- Tissue-specific activation of tumor marker glutathione transferase P transgenes in transgenic rats.Journal of cancer research and clinical oncology · 1995Article
- Expression of human tyrosine hydroxylase-chloramphenicol acetyltransferase (CAT) fusion gene in the brains of transgenic mice as examined by CAT immunocytochemistry.Journal of neural transmission. General section · 1994Article
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9 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Glutathione transferase P (GST-P; glutathione transferase, EC 2.5.1.18) is known to be specifically expressed at high levels in precancerous lesions and in hepatocellular carcinomas from a very early phase of chemically induced hepatocarcinogenesis in the rat. The almost invariable occurrence of this phenotype in these lesions strongly suggests a mechanism by which GST-P gene is activated together with a crucial transforming gene of liver cells. To distinguish the two alternative possibilities--either the GST-P gene is coactivated with a closely located transforming gene by a cis mechanism or it is activated in trans by a common trans-acting factor--we carried out carcinogenesis experiments using transgenic rats harboring the bacterial chloramphenicol acetyltransferase reporter gene ligated to the upstream regulatory sequence of the GST-P gene. In each of three independent lines tested, liver foci and nodules produced by chemical carcinogens (Solt-Farber procedure) were found to express high levels of chloramphenicol acetyltransferase activity, indicating clearly that the GST-P gene is activated by a trans mechanism during hepatocarcinogenesis.
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