ArticleProceedings of the National Academy of Sciences of the United States of America1996
Two genes abrogate the inhibition of murine hepatocarcinogenesis by ovarian hormones.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 47 citations in OpenAlex.
- Review
- The role for estrogen receptor-alpha and prolactin receptor in sex-dependent DEN-induced liver tumorigenesis.Carcinogenesis · 2011Article
- Predominant modifier of extreme liver cancer susceptibility in C57BR/cdJ female mice localized to 6 Mb on chromosome 17.Carcinogenesis · 2009Article
- Interaction of major genes predisposing to hepatocellular carcinoma with genes encoding signal transduction pathways influences tumor phenotype and prognosis.World journal of gastroenterology · 2008Article
- Frequent trefoil factor 3 (TFF3) overexpression and promoter hypomethylation in mouse and human hepatocellular carcinomas.International journal of oncology · 2005Article
- SOCS1 is a suppressor of liver fibrosis and hepatitis-induced carcinogenesis.The Journal of experimental medicine · 2004Article
- A potent modifier of liver cancer risk on distal mouse chromosome 1: linkage analysis and characterization of congenic lines.Genetics · 2004Article
- Article
- Circadian expression of the steroid 15 alpha-hydroxylase (Cyp2a4) and coumarin 7-hydroxylase (Cyp2a5) genes in mouse liver is regulated by the PAR leucine zipper transcription factor DBP.Molecular and cellular biology · 1999Article
- Genetic identification of multiple loci that control breast cancer susceptibility in the rat.Genetics · 1998Article
- Genetic basis of sex-specific resistance to neuro-oncogenesis in (BDIX x BDIV) F(2) rats.Mammalian genome : official journal of the International Mammalian Genome SocietyArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hormonal and genetic factors strongly influence the susceptibility of inbred mice to hepatocarcinogenesis. Female C57BR/cdJ (BR) mice are extremely susceptible to liver tumor induction relative to other strains because they are genetically insensitive to the inhibition of hepatocarcinogenesis by ovarian hormones. To determine the genetic basis for the sensitivity of BR mice relative to resistant C57BL/6J (B6) mice, we treated 12-day-old B6BRF1 x B6 and B6BRF1 x B6BRF1 (F2) animals with N,N-diethylnitrosamine (0.1 micromol/g of body weight) and enumerated liver tumors at 32 weeks of age in males and at 50 weeks in females. Genomic DNA samples from backcross and F2 mice were analyzed for 70 informative simple sequence length polymorphism markers. Genetic markers on chromosome 17 (D17Mit21) and chromosome 1 (D1Mit33) cosegregated with high tumor multiplicity in both sexes. Together, these loci [designated Hcf1 and Hcf2 (Hepatocarcinogenesis in females), respectively] account for virtually all of the difference in sensitivity between BR and B6 mice. The Hcf1 locus accounts for a majority of the higher susceptibility of BR mice of both sexes. Backcross female mice heterozygous at both loci (33 +/- 23 tumors per mouse) and at Hcf1 only (17 +/- 18) were 15- and 8-fold more sensitive, respectively, than mice homozygous for the B6 alleles at Hcf1 and Hcf2 (2.2 +/- 3.9). In backcross male mice, the double heterozygotes (35 +/- 22) and Hcf1 heterozygotes (28 +/- 12) were 5.4- and 4.3-fold more sensitive than mice homozygous for B6 alleles at both loci (6.5 +/- 5.4).
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