Journal
CANCER LETTERS
Volume 317, Issue 2, Pages 226-236Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2011.11.031
Keywords
E6E7; HPV; Retinoid receptor; Cervical cancer; Murine models
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Funding
- CONACyT (Mexico)
- ICGEB
- UICC
- Novartis (Switzerland)
- Ligue Contre le Cancer comite de Bas-Rhin
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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 RXR alpha 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. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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