ArticleGenetics1995
Identification of hepatocarcinogen-resistance genes in DBA/2 mice.
Article in Genetics, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 74 citations in OpenAlex.
- In Vivo and In Vitro Models of Hepatocellular Carcinoma: Current Strategies for Translational Modeling.Cancers · 2021Review
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- Genetic background determines if Stat5b suppresses or enhances murine hepatocarcinogenesis.Molecular carcinogenesis · 2015Article
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- Biological Basis of Differential Susceptibility to Hepatocarcinogenesis among Mouse Strains.Journal of toxicologic pathology · 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
- Genome-level analysis of genetic regulation of liver gene expression networks.Hepatology (Baltimore, Md.) · 2007Article
- Genetic linkage between Pol iota deficiency and increased susceptibility to lung tumors in mice.Cancer science · 2005Article
- A potent modifier of liver cancer risk on distal mouse chromosome 1: linkage analysis and characterization of congenic lines.Genetics · 2004Article
- Different genetic control of cutaneous and visceral disease after Leishmania major infection in mice.Infection and immunity · 2003Article
- Fine chromosomal localization of the mouse Par2 gene that confers resistance against urethane-induction of pulmonary adenomas.Oncogene · 2001Article
- A subset of skin tumor modifier loci determines survival time of tumor-bearing mice.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Nonrandom cytogenetic alterations in hepatocellular carcinoma from transgenic mice overexpressing c-Myc and transforming growth factor-alpha in the liver.The American journal of pathology · 1999Article
- alpha-Fetoprotein gene sequences mediating Afr2 regulation during liver regeneration.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Mouse mammary tumor virus/v-Ha-ras transgene-induced mammary tumors exhibit strain-specific allelic loss on mouse chromosome 4.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Two genes abrogate the inhibition of murine hepatocarcinogenesis by ovarian hormones.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Conditional transformation of mouse liver epithelial cells. An in vitro model for analysis of genetic events in hepatocarcinogenesis.The American journal of pathology · 1995Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Male DBA/2J mice are approximately 20-fold more susceptible than male C57BL/6J mice to hepatocarcinogenesis induced by perinatal treatment with N,N-diethylnitrosamine (DEN). In order to elucidate the genetic control of hepatocarcinogenesis in DBA/2J mice, male BXD recombinant inbred, D2B6F1 x B6 backcross, and D2B6F2 intercross mice were treated at 12 days of age with DEN and liver tumors were enumerated at 32 weeks. Interestingly, the distribution of mean tumor multiplicities among BXD recombinant inbred strains indicated that hepatocarcinogen-sensitive DBA/2 mice carry multiple genes with opposing effects on the susceptibility to liver tumor induction. By analyzing D2B6F1 x B6 backcross and D2B6F2 intercross mice for their liver tumor multiplicity phenotypes and for their genotypes at simple sequence repeat marker loci, we mapped two resistance genes carried by DBA/2J mice, designated Hcr1 and -2, to chromosomes 4 and 10, respectively. 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 the backcross population. Although our collection of 100 simple sequence repeat markers allowed linkage analysis for approximately 95% of the genome, we failed to map any sensitivity alleles for DBA/2J mice. Thus, it is likely that the susceptibility of DBA/2J mice is the consequence of the combined effects of multiple sensitivity loci.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.