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Mutational activation of the c-Ha-ras gene in liver tumors of different rodent strains: correlation with susceptibility to hepatocarcinogenesis.
TLDR
Results indicate a close correlation between the mutational activation of the c-Ha-ras gene in liver tumors of the different rodent strains and their susceptibility to hepatocarcinogenesis, whereby the mutations appear to provide a selective growth advantage, leading to a clonal expansion of the mutated liver cell population, only in livers of sensitive but not of insensitive strains.
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Hepatocarcinogenicity of estragole (1-allyl-4-methoxybenzene) and 1'-hydroxyestragole in the mouse and mutagenicity of 1'-acetoxyestragole in bacteria.
TLDR
Estragole induced hepatocellular carcinomas by 15 months in 23 and 39% of the mice that received total doses of 4.4 and 5.2 mumoles, respectively, and lived to an age of 12 months or more, and 1'-Acetoxyallybenzene had little or no activity in either of these tests.
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Rapid growth of preneoplastic lesions in hepatocarcinogen-sensitive C3H/HeJ male mice relative to C57BL/6J male mice.
TLDR
The phenotypic effect of the Hcs locus appears to be dependent on promotion of liver tumor induction by the male hormonal environment and may affect the promotion phase of hepatocarcinogenesis in male mice by increasing the proliferative rate of both normal and preneoplastic hepatocytes.
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Genetic control of hepatocarcinogenesis in C57BL/6J and C3H/HeJ inbred mice.
TLDR
Analysis of DEN-induced liver tumor multiplicities as a quantitative genetic trait in segregating crosses between C3H/HeJ and C57BL/6J mice indicated that allelic differences for at least two loci contributed to the higher sensitivity to hepatocarcinogenesis of C3h/Hej mice relative to C57bl/ 6J mice.
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Genetic dissection of susceptibility to murine ovarian teratomas that originate from parthenogenetic oocytes.
TLDR
A locus on chromosome 6 designated Ots1 (ovarian teratoma susceptibility) was identified as the single major locus that increases the frequency of teratomas in a semidominant manner.
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Two genes abrogate the inhibition of murine hepatocarcinogenesis by ovarian hormones.
TLDR
The Hcf1 locus accounts for a majority of the higher susceptibility of BR mice of both sexes, and together, these loci account for virtually all of the difference in sensitivity between BR and B6 mice.
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Liver tumor promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxin is dependent on the aryl hydrocarbon receptor and TNF/IL-1 receptors.
TLDR
The idea that the mechanism of dioxin acute hepatotoxicity and its activity as a promoter in a mouse two stage liver cancer model may be similar is supported, i.e., tumor promotion bydioxin, like acute hepatOToxicity, are mediated by the linked action of two receptor systems, the AHR and the receptors for the "IL-1-like" cytokines.
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Genetic control of hepatocarcinogenesis in C3H mice.
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Identification of hepatocarcinogen-resistance genes in DBA/2 mice.
TLDR
Analysis of DBA/2J mice for their liver tumor multiplicity phenotypes and for their genotypes at simple sequence repeat marker loci indicated that Hcr1 and Hcr2 resolved the genetic variance in the backcross population well, indicating that these resistance loci are the major determinants of the variance in that population.
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Genetic variation in liver tumor susceptibility, plasma testosterone levels, and androgen receptor binding in six inbred strains of mice.
TLDR
Variation in testosterone levels among the different strains of mice was not correlated with liver tumor susceptibility and the presence of high affinity androgen receptors in mouse hepatic cytosol was demonstrated.
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