Evaluation of c-K-ras in pancreatic carcinomas from Ela-1, SV40E transgenic mice

c-K-ras is activated by mutation at codon 12 in the majority of human pancreatic carcinomas of ductal, but not acinar, phenotype. Therefore, evaluation of c-K-ras in experimentally induced pancreatic carcinomas in animal models is of interest for comparison with the human disease. Acinar cell carcin...

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Bibliographic Details
Published in:Carcinogenesis (New York) 1993-12, Vol.14 (12), p.2649-2651
Main Authors: Kuhlmann, Elna, Terhune, Pamela Guay, Longnecker, Daniel S.
Format: Article
Language:English
Subjects:
Animal tumors. Experimental tumors
Animals
Biological and medical sciences
Disease Models, Animal
Experimental digestive system and abdominal tumors
Female
Genes, ras
Male
Medical sciences
Mice
Mice, Transgenic
Mutation
Pancreatic Neoplasms - genetics
Polymerase Chain Reaction
Tumors
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Summary:c-K-ras is activated by mutation at codon 12 in the majority of human pancreatic carcinomas of ductal, but not acinar, phenotype. Therefore, evaluation of c-K-ras in experimentally induced pancreatic carcinomas in animal models is of interest for comparison with the human disease. Acinar cell carcinomas and islet cell tumors arising in two strains of transgenic mice carrying the Ela-1-SV40E transgene were evaluated using the polymerase chain reaction and allele specific oligomer hybridization to seek evidence of c-K-ras mutation at codons 12, 13 and 61. Amplified DNA products, including codons 12 and 13, from the majority of these tumors were also evaluated by single strand conformation polymorphism analysis. Only wild type c-K-ras was found in the tumors.
ISSN:0143-3334
1460-2180
DOI:10.1093/carcin/14.12.2649