Genetic changes during mouse skin tumorigenesis.
This paper describes specific genetic changes involving chromosome 7 in mouse skin tumors, the most important consequence of which appears to be an alteration in the allelic balance of normal and mutant H-ras genes. The use of restriction-fragment-length polymorphisms in F1 hybrid mice demonstrates that trisomy of chromosome 7 is an early event preceding papilloma formation, and further events, such as mitotic recombination, seem to occur during progression to malignant carcinomas. There is some evidence of a tumor-suppressor locus situated on chromosome 7.
Beatson Institute for Cancer Research, Glasgow, UK.
P A
PA
Burns
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R
Bremner
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Balmain
D000483:Alleles; D000818:Animals; D002277:Carcinoma / Q000139:chemically induced / Q000235:genetics*; D002875:Chromosomes / Q000187:drug effects / Q000648:ultrastructure; D004249:DNA Damage; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D016147:Genes, Tumor Suppressor; D011905:Genes, ras; D006824:Hybridization, Genetic; D008769:Methylnitronitrosoguanidine; D051379:Mice; D010212:Papilloma / Q000139:chemically induced / Q000235:genetics*; D012150:Polymorphism, Restriction Fragment Length; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics*; D011995:Recombination, Genetic; D012878:Skin Neoplasms / Q000139:chemically induced / Q000235:genetics*; D014314:Trisomy
D008769:Methylnitronitrosoguanidine; D016283:Proto-Oncogene Proteins p21(ras)