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Cancer Lett. 2012 Apr 28;317(2):226-36. doi: 10.1016/j.canlet.2011.11.031. Epub 2011 Nov 29.

RXRα deletion and E6E7 oncogene expression are sufficient to induce cervical malignant lesions in vivo.

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  • 1Dept. of Genetics & Molecular Biology, Centro de Investigacion y de Estudios Avanzados del IPN (CINVESTAV-IPN). Av. IPN 2508, Col. San Pedro Zacatenco, 07360. Mexico, DF, Mexico.


Cervical cancer is the second leading cause of cancer deaths among women worldwide. High-Risk-Human Papillomaviruses (HR-HPVs) play an important etiologic role in the development of carcinoma of the uterine cervix. However, host factors are important in determining the outcome of genital HPV infection as most cervical precancerous lesions containing HR-HPVs do not progress to invasive carcinomas. Retinoids, acting through nuclear receptors (RARs, RXRs), play a crucial role in cervix development and homeostasis regulating growth and differentiation of a wide variety of cell types; indeed, they can inhibit cell proliferation, and induce cell differentiation or apoptotic cell death. Here we introduce a mouse model that develops spontaneously malignant cervical lesions allowing the study of the cooperative effect between HPV16E6E7 expression and the lack of RXRα in cervical cancer development. This model could be useful to study multistep carcinogenesis of uterine cervix tissue and might improve chemopreventive and chemotherapeutic strategies for this neoplasia.

Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

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