ArticleJapanese journal of cancer research : Gann1992
Phenotypic properties of liver tumors induced by dehydroepiandrosterone in F-344 rats.
Article in Japanese journal of cancer research : Gann, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Modulation of dihydroxy-di-n-propylnitrosamine-induced liver lesion development in Opisthorchis-infected Syrian hamsters by praziquantel treatment in association with butylated hydroxyanisole or dehydroepiandrosterone administration.Japanese journal of cancer research : Gann · 1998Article
- Fish models for environmental carcinogenesis: the rainbow trout.Environmental health perspectives · 1996Review
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5 authors at 1 institution in 1 country.
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Abstract
Dehydroepiandrosterone (DHEA), a C19 adrenal steroid hormone, induces peroxisome proliferation in liver cells and is hepatocarcinogenic in the rat. The present study deals with the phenotypic properties of DHEA-induced liver lesions. A majority of the altered areas (80-87%), neoplastic nodules (> 94%) and hepatocellular carcinomas (HCC, 80-100%) lacked the marker enzymes gamma-glutamyltranspeptidase and placental form of glutathione S-transferase (GSTP). Northern blot analysis of HCC from 4 rats revealed no detectable GSTP mRNA. These HCC, however, showed a marked decrease in the staining of glucose-6-phosphatase and adenosine triphosphatase. These results indicate that the phenotypic properties of liver tumors induced by DHEA and amphipathic carboxylate peroxisome proliferators are similar.
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