Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (43)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by van Kranen, H.J.
Right arrow Articles by Scherer, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van Kranen, H.J.
Right arrow Articles by Scherer, E.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1991 Oxford University Press

research-article

Activation of c-K-ras is frequent in pancreatic carcinomas of Syrian hamsters, but is absent in pancreatic tumors of rats

H.J. van Kranen, E. Vermeulen 1, L. Schoren, J. Bax 1, R.A. Woutersen 2, P. van Iersel, C.F. van Kreiji and E. Scherer 1

Laboratory of Carcinogenesis and Mutagenesis, National Institute of Public Health and Environmental Protection PO Box I, 3720 BA Bilthoven
1Division of Chemical Carcinogenesis, The Netherlands Cancer Institute (Antoni van Leeuwenhockhuis) Plesmanlaan 121, 1066 CX Amsterdam
2Department of Biological Toxicology, TNO-CIVO Toxicology and Nutrition Institute Zeist, The Netherlands

We have investigated the presence of mutations in ras genes at codons 12, 13 and 61 in chemically induced pancreatic tumors of rats and Syrian hamsters. Mutations were detected by means of allele-specific oligonucleotide hybridization to ras sequences, amplified in vitro by the polymerase chain reaction. No mutations were observed in the c-K-ras gene or the c-H-ras gene of nine azaserine-induced adenomas and 15 carcinomas of the rat pancreas. This indicates that activated ras genes are not commonly involved in rat pancreatic cancer evolving from acinar cells. However, in 19 out of 20 ductular adenocarcinomas of hamster pancreas (95%), either codon 12 or 13 of the c-K-ras gene was mutated. This indicates that the activation of c-K-ras is a frequent event in the multistep process of pancreatic carcinogenesis induced by the alkylating carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). The mutations of both codons were G->A transitions of the second base which is consistent with the type of mutation to be expected from DNA alkylation. Activation of the c-K-ras gene, therefore, may not only be a frequent but also an early event in hamster pancreas carcinogenesis. The frequent activation of the c-K-ras gene in both human and hamster pancreatic cancer emphasizes the relevance of BOP-induced pancreatic adenocarcinomas in Syrian hamsters as an experimental model system for studying human pancreatic cancer.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
J. Li, C. M. Weghorst, M. Tsutsumi, M. J. Poi, T. J. Knobloch, B. C. Casto, W. S. Melvin, M.-D. Tsai, and P. Muscarella
Frequent p16INK4A/CDKN2A alterations in chemically induced Syrian golden hamster pancreatic tumors
Carcinogenesis, February 1, 2004; 25(2): 263 - 268.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.