Initiation of chemical carcinogenesis requires cell proliferation

Cayama, Edmundo; Tsuda, Hiroyuki; Sarma, D.S.R.; Farber, Emmanuel

doi:10.1038/275060a0

Cited by 300 publications

(75 citation statements)

References 12 publications

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“…Adult liver is a stable, quiescent tissue, but it responds to partial hepatectomy or hepatocyte necrosis with increased cell proliferation. Because of its remarkable regenerative capacity the rat liver has proven to be an excellent model for studies of cell proliferation and carcinogenesis (Cayama et al, 1978;Kaufmann et al, 1981). In spite of an extensive literature on hepatocarcinogenesis, there are few reports on telomeres and telomerase activity in normal rat liver and liver tumors (Makarov et al, 1993;Yoshimi et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Expression of telomerase in normal and malignant rat hepatic epithelia

et al. 1997

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Section: Introductionmentioning

confidence: 99%

Expression of telomerase in normal and malignant rat hepatic epithelia

et al. 1997

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“…40) Colchicine at a dose of 0.5 mg/kg body weight was injected intraperitoneally 1 and 3 days after DEN treatment. After an 11-day recovery period, rats were placed on the selection regimen, comprising feeding of 0.02% AAF diet for 2 weeks and a single intragastric administration of CCl 4 at 1 ml/kg body weight, following the procedure described by Cayama et al, 41) and were killed under ether anesthesia 42 weeks after the beginning of the experiment. Liver samples At sacrifice, the livers were immediately excised and grossly apparent tumors were dissected from surrounding tissue.…”

Section: Animalsmentioning

confidence: 99%

Alterations of the Transforming Growth Factor‐(β Signaling Pathway in Hepatocellular Carcinomas Induced Endogenously and Exogenously in Rats

Sasaki

Tsujiuchi

Murata

et al. 2001

Japanese Journal of Cancer Research

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“…Although not a sufficient condition (8,9), cell division seems to be a prerequisite in a number of stages in the process of carcinogenesis. Firstly, the replication of damaged DNA is a necessary event for a successful initiation (10)(11)(12)(13). Secondly, the mitotic activity plays an important role during the period of tumor promotion and progression (14).…”

Section: Introductionmentioning

confidence: 99%

Stimulation of DNA synthesis in rat and mouse liver by various tumor promoters

Büsser

Lutz

1987

Carcinogenesis

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'To whom reprint requests should be sentIn order to investigate whether the stimulation of liver DNA synthesis might be used to detect one class of hepatic tumor promoters, the incorporation of orally administered radiolabelled thymidine into liver DNA was determined in rats and mice 24 h after a single oral gavage of test compounds at various dose levels. Three DNA-binding hepatocarcinogens, aflatoxin B,~ benzidine and carbon tetrachloride, did not stimulate but rather inhibited DNA synthesis (not for CC1 4 ). Four hepatic tumor promoters, clofibrate, DDT, phenobarbital and thioacetamide, gave rise to a stimulation in a dosedependent manner. Single oral doses between 0.02 and 0.3 mmol/kg were required to double the level of thymidine incorporation into liver DNA (= doubling dose, DD). Differences between species or sex as observed in long-term carcinogenicity studies were reflected by a different stimulation of liver DNA synthesis. In agreement with the bioassay data, aldrin was positive only in male mice (DD = 0.007 mmol/kg) but not in male rats or female mice. 2,3,7,8-TCDD was positive in male mice (DD = 10 ~6 mmol/kg) and in female rats (DD = 2 x 10~6 mmol/kg) but not in male rats. The assay was also able to distinguish between structural isomers with different carcinogenicities.[alpha] Hexachlorocyclohexane stimulated liver DNA synthesis with a doubling dose of about 0.2 mmol/kg in male rats whereas the [gamma]-isomer was ineffective even at 1 mmol/kg. So far, only one result was inconsistent with carcinogenicity bioassay data. The different carcinogenicity of di(2-ethylhexyl)adipate (negative in rats) and di(2-ethylhexyl)phthalate (positive) was not detectable. Both plasticizers were positive in this short-term system with DD's of 0.7 mmol/kg for DEHA and 0.5 mmol/kg for DEHP. The proposed assay is discussed as an attempt to devise short-term assays for carcinogens not detected by the routine genotoxicity test systems.

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Initiation of chemical carcinogenesis requires cell proliferation

Cited by 300 publications

References 12 publications

Expression of telomerase in normal and malignant rat hepatic epithelia

Expression of telomerase in normal and malignant rat hepatic epithelia

Alterations of the Transforming Growth Factor‐(β Signaling Pathway in Hepatocellular Carcinomas Induced Endogenously and Exogenously in Rats

Stimulation of DNA synthesis in rat and mouse liver by various tumor promoters

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