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Tumor formation in p53 mutant ovaries transplanted into wild-type female hosts

Oncogene volume 23, pages 7722–7725 (2004)Cite this article

Abstract

p53 gene alterations correlate highly with advanced ovarian carcinoma in women. In mice, p53 deficiency predominantly results in the formation of lymphomas and sarcomas. However, ovarian epithelial tumors have not been documented in p53 homozygous mutant (p53−/−) mice, probably because they die before other tumors can form. To determine whether p53−/− ovaries can develop epithelial tumors, they were transplanted into the ovarian bursae of histocompatible wild-type recipient females. The p53−/− ovarian grafts formed tumors ∼1 year post-transplantation. The tumor type was angiosarcoma, suggesting that vascular tissues are predisposed to tumor formation in p53−/−ovaries. These findings suggest that p53 deficiency alone is not sufficient for ovarian epithelial tumorigenesis in mice. Thus, other genetic lesions are likely required to develop mouse models of human ovarian cancer.

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Acknowledgements

This work was supported by a Development Grant from the National Cancer Institute Specialized Programs of Research Excellence in Ovarian Cancer (CA83639) and grants from the National Institutes of Health (NIH) (HD30284) and Department of Defense Ovarian Cancer Research Program (OC020187) to RRB. Veterinary resources were supported by the NIH Cancer Center Support (Core) Grant CA16672.

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  1. Chun-Ming Chen

    Present address: Faculty of Life Sciences, National Yang-Ming University, Taipei, 112, Taiwan

Authors and Affiliations

  1. Department of Molecular Genetics, University of Texas, MD Anderson Cancer Center, Houston, TX, USA

    Chun-Ming Chen & Richard R Behringer

  2. Department of Pathology, Armed Forced Taoyuan General Hospital, Taoyuan County, Taiwan

    Junn-Liang Chang

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  1. Chun-Ming Chen
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  2. Junn-Liang Chang
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Correspondence to Richard R Behringer.

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Chen, CM., Chang, JL. & Behringer, R. Tumor formation in p53 mutant ovaries transplanted into wild-type female hosts. Oncogene 23, 7722–7725 (2004). https://doi.org/10.1038/sj.onc.1208037

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