Induction of carcinogenesis by concurrent inactivation of p53 and Rb1 in the mouse ovarian surface epithelium

Alterations in p53 and Rb pathways are observed frequently in epithelial ovarian cancer (EOC).However, their roles in EOC initiation remain uncertain. Using a single intrabursal administration of recombinant adenovirus expressing Cre, we demonstrate that concurrent inactivation of p53 and Rb1 is suf...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2003-07, Vol.63 (13), p.3459-3463
Main Authors: FLESKEN-NIKITIN, Andrea, CHOI, Kyung-Chul, ENG, Jessica P, SHMIDT, Elena N, NIKITIN, Alexander Yu
Format: Article
Language:English
Subjects:
Adenoviridae - genetics
Animals
Biological and medical sciences
Cell Survival
Cell Transformation, Neoplastic - genetics
Cells, Cultured
DNA Primers
Epithelial Cells - cytology
Epithelial Cells - pathology
Epithelial Cells - physiology
Female
Genes, p53
Genes, Reporter
Genes, Retinoblastoma
Medical sciences
Mice
Mice, Transgenic
Ovarian Neoplasms - genetics
Ovary - pathology
Polymerase Chain Reaction
Rb1 gene
Retinoblastoma Protein - antagonists & inhibitors
Transfection
Tumor Suppressor Protein p53 - antagonists & inhibitors
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Summary:Alterations in p53 and Rb pathways are observed frequently in epithelial ovarian cancer (EOC).However, their roles in EOC initiation remain uncertain. Using a single intrabursal administration of recombinant adenovirus expressing Cre, we demonstrate that concurrent inactivation of p53 and Rb1 is sufficient for reproducible induction of ovarian epithelial carcinogenesis in mice homozygous for conditional gene alleles. Similarly to progression of disease in women, ovarian neoplasms spread i.p., forming ascites, and metastasize to the contralateral ovary, the lung, and the liver. These results establish critical interactions between p53 and Rb1 pathways in EOC pathogenesis, and provide a genetically defined immunocompetent mouse model of sporadic EOC.
ISSN:0008-5472
1538-7445