ArticleComparative biochemistry and physiology. Toxicology & pharmacology : CBP2009
Etiology of MNU-induced melanomas in Xiphophorus hybrids.
Article in Comparative biochemistry and physiology. Toxicology & pharmacology : CBP, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The Power of Fish Models to Elucidate Skin Cancer Pathogenesis and Impact the Discovery of New Therapeutic Opportunities.International journal of molecular sciences · 2018Review
- Molecular genetic response of Xiphophorus maculatus-X. couchianus interspecies hybrid skin to UVB exposure.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2015Article
- N-Methyl-N-nitrosourea as a mammary carcinogenic agent.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Recent advances in sunlight-induced carcinogenesis using the Xiphophorus melanoma model.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2012Article
- Genetic and environmental melanoma models in fish.Pigment cell & melanoma research · 2010Review
- Aquatic animal models of human disease: selected papers and recommendations from the 4th Conference.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2009Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Genetic hybrids of the genus Xiphophorus have historically been useful models for study of the genetic aspects of tumor formation. In the most studied Xiphophorus tumor model, two-gene loci, XMRK and DIFF, are implicated as critical both to UV-induced and spontaneous melanoma formation in BC(1) hybrids of crosses between X. maculatus and X. helleri, with X. helleri as the recurrent backcross parent. In addition to UV, the direct-acting carcinogen N-methyl-N-nitrosourea (MNU) has been used to induce tumors in Xiphophorus BC(1) hybrids from several cross types. In the present study, we address the hypothesis that excess melanomas in MNU-treated BC(1) hybrids may have been generated by direct mutation of CDKN2AB, a candidate gene for DIFF. MNU treatment of F(1) and BC(1) hybrid fish significantly increased tumor incidence at 6 months; however, no association was found between MNU-induced tumor formation and zygosity of the candidate tumor tumor-suppressor CDKN2AB in BC(1) hybrids, consistent with previously reported results. Sequence analysis of the X. maculatus CDKN2AB locus of heterozygous individuals (both BC(1) and F(1) hybrids) did not reveal any mutations caused by MNU, suggesting that the mechanism of MNU-induced melanoma formation in this Xiphophorus model does not involve direct mutation of CDKN2AB but may result from mutation of other critical genes.
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