Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
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 (3)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Hulla, J. E.
Right arrow Articles by Dunnick, J. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hulla, J. E.
Right arrow Articles by Dunnick, J. K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Toxicological Sciences 60, 264-270 (2001)
Copyright © 2001 by the Society of Toxicology

CARCINOGENICITY

Chromosome 11 Loss from Thymic Lymphomas Induced in Heterozygous Trp53 Mice by Phenolphthalein

Janis E. Hulla*,1, John E. French{dagger} and June K. Dunnick{dagger}

* University of North Dakota School of Medicine, Grand Forks, ND; and {dagger} National Institute of Environmental Health Sciences, Research Park, North Carolina 27709

C57BL/6 p53 (+/–) N5 mice heterozygous for a null p53 allele were given phenolphthalein to learn more about mechanisms of carcinogenesis and to evaluate the p53-deficient mouse as a tool for identifying potential human carcinogens. DNA samples isolated from 10 phenolphthalein-induced thymic lymphomas were analyzed for loss of heterozygosity (LOH) at the Trp53 locus and simple sequence length polymorphic (SSLP) loci. The initial screening revealed remarkable results from only chromosome 11. Allelotyping at approximately five centiMorgan intervals, we found SSLP heterozygosity for C57BL/6 and 129Sv over much of chromosome 11. In the tumors, treatment-related LOH was apparent on chromosome 11 at each of the 28 informative loci examined. The strain-specific polymorphism lost from individual tumors allowed us to deduce the distribution of alleles along the length of the maternal and paternal chromosomes 11. The allelic patterns indicate that mitotic homologous recombination occurred during embryogenesis if breeding protocols were carried out as described. The mitotic recombination observed may be attributable to p53 haploinsufficiency for normal suppression of mitotic recombination.

Key Words: allelotype; simple sequence length polymorphism; SSLP; carcinogenesis; thymus; lymphoma; phenolphthalein; recombination; LOH; chromosome loss..


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
 Cancer Res.Home page
A. Karlsson, P. Soderkvist, and S.-M. Zhuang
Point Mutations and Deletions in the Znfn1a1/Ikaros Gene in Chemically Induced Murine Lymphomas
Cancer Res., May 1, 2002; 62(9): 2650 - 2653.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol PatholHome page
J. French, R. D. Storer, and L. A. Donehower
The Nature of the Heterozygous Trp53 Knockout Model for Identifi cation of Mutagenic Carcinogens
Toxicol Pathol, January 1, 2001; 29(1_suppl): 24 - 29.
[Abstract] [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.