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(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.




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