Carcinogenesis, Vol. 20, No. 8, 1397-1402,
August 1999
© 1999 Oxford University Press
Commentaries |
Cytokines in non-genotoxic hepatocarcinogenesis
Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield SK10 4TJ, UK
Abbreviations: FADD, Fas-activated death domain; HBV, hepatitis B virus; IL, interleukin; PB, phenobarbitone; PPs, peroxisome proliferators; PPAR
, peroxisome proliferator-activated receptor; RIP, receptor-interacting protein; STAT, signal transducers and activators of transcription; TNF, tumour necrosis factor ; TNFR, tumour necrosis factor receptor; TRADD, TNFR1-associated death domain
Non-genotoxic liver injury
Many toxicants can cause liver injury. Some, such as diethylnitrosamine, are genotoxic and act principally by damaging DNA (1). A second more diverse group cause liver injury but are non-genotoxic (2). Despite differences in the primary target, genotoxic and non-genotoxic hepatotoxicants frequently cause tumours in the liver of experimental rats and mice (1,2). This review is concerned with evaluating the hypothesis that cytokines may play a role in mediating the biological effects of liver non-genotoxic carcinogens.
Non-genotoxic liver toxicants constitute a diverse group of chemicals. Some, such as carbon tetrachloride (3), cause acute liver injury followed by regenerative hyperplasia, whereas others cause proliferation without identifiable tissue damage. The latter group includes barbiturate drugs such as phenobarbitone (PB) (4), dioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (5,6) and the largest group, the peroxisome proliferators (PPs) (
TNF-: role in non-genotoxic liver injury
Evidence for a cytokine signalling network
Cytokines, viral hepatitis and hepatocellular carcinoma
Summary and future directions
Notes
References
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