help button home button Am J Pathol ASIP 2008 Summer Academy, Molecular Methcanisms of Human Disease: Injury, Inflammation, and Tissue Repair
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Politi, K.
Right arrow Articles by Efstratiadis, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Politi, K.
Right arrow Articles by Efstratiadis, A.
(American Journal of Pathology. 2004;164:325-336.)
© 2004 American Society for Investigative Pathology

Animal Model

A Mouse Model of Uterine Leiomyosarcoma

Katerina Politi*, Matthias Szabolcs{dagger}, Peter Fisher{dagger}, Ana Kljuic*, Thomas Ludwig§{ddagger} and Argiris Efstratiadis*{ddagger}

From the Departments of Genetics and Development,* Pathology,{dagger} and Anatomy and Cell Biology,§ and the Institute for Cancer Genetics,{ddagger} Columbia University, New York, New York

We are using an approach that is based on the cre/loxP recombination process and involves a binary system of Cre-producing and Cre-responding transgenic mice to achieve ubiquitous or tissue-specific expression of oncoproteins. To develop mouse models of tumorigenesis, Cre-producers are mated with responder animals carrying a dormant oncogene targeted into the 3' untranslated region of the locus encoding cytoplasmic ß-actin (actin cassette). Production of oncoprotein from a bicistronic message is accomplished in bitransgenic progeny by Cre-mediated excision of a segment flanked by loxP sites that is located upstream from the oncogenic sequence. Widespread Cre-dependent activation and expression of an actin-cassette transgene encoding the T antigens of the SV40 early region (SVER) commencing in embryos was compatible with normal development and did not impair viability. However, at ~3 months of age, all female animals developed massive uterine leiomyosarcomas, whereas practically all males exhibited enormously enlarged seminal vesicles because of pronounced hyperplasia of the smooth muscle layers. In addition, because of smooth muscle hyperproliferation, marked dilation of the gallbladder was observed in mice of both sexes. To begin exploring aberrant signaling events in the SVER-triggered tumorigenic pathways, we analyzed the expression profile of leiomyosarcomas by DNA microarray analysis.




This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
A. Klinakis, M. Szabolcs, K. Politi, H. Kiaris, S. Artavanis-Tsakonas, and A. Efstratiadis
From the Cover: Myc is a Notch1 transcriptional target and a requisite for Notch1-induced mammary tumorigenesis in mice
PNAS, June 13, 2006; 103(24): 9262 - 9267.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
M. R. Schneider, M. Dahlhoff, N. Herbach, I. Renner-Mueller, C. Dalke, O. Puk, J. Graw, R. Wanke, and E. Wolf
Betacellulin Overexpression in Transgenic Mice Causes Disproportionate Growth, Pulmonary Hemorrhage Syndrome, and Complex Eye Pathology
Endocrinology, December 1, 2005; 146(12): 5237 - 5246.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the American Society for Investigative Pathology.