Document Detail


RXRα deletion and E6E7 oncogene expression are sufficient to induce cervical malignant lesions in vivo.
MedLine Citation:
PMID:  22138104     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Rodolfo Ocadiz-Delgado; Eduardo Castañeda-Saucedo; Arup K Indra; Rogelio Hernandez-Pando; Pedro Flores-Guizar; Jose Luis Cruz-Colin; Felix Recillas-Targa; Guillermo Perez-Ishiwara; Luis Covarrubias; Patricio Gariglio
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-11-29
Journal Detail:
Title:  Cancer letters     Volume:  317     ISSN:  1872-7980     ISO Abbreviation:  Cancer Lett.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-02-10     Completed Date:  2012-04-17     Revised Date:  2012-10-09    
Medline Journal Info:
Nlm Unique ID:  7600053     Medline TA:  Cancer Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  226-36     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
Dept. 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.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / genetics
Cell Proliferation
Cell Transformation, Neoplastic / genetics*,  metabolism,  pathology
Cervix Uteri / metabolism*,  pathology
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism
Female
Gene Expression Regulation, Neoplastic
Humans
Immunohistochemistry
Mice
Mice, Knockout
Mice, Transgenic
Models, Genetic
Oncogene Proteins, Viral / genetics*,  metabolism
Proto-Oncogene Proteins c-bcl-2 / genetics,  metabolism
Proto-Oncogene Proteins c-myc / genetics,  metabolism
Repressor Proteins / genetics*,  metabolism
Retinoid X Receptor alpha / genetics*,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Uterine Cervical Neoplasms / genetics*,  metabolism,  pathology
bcl-2-Associated X Protein / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
R01 ES016629/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Cdkn1a protein, mouse; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/E6 protein, Human papillomavirus type 16; 0/Myc protein, mouse; 0/Oncogene Proteins, Viral; 0/Proto-Oncogene Proteins c-bcl-2; 0/Proto-Oncogene Proteins c-myc; 0/Repressor Proteins; 0/Retinoid X Receptor alpha; 0/bcl-2-Associated X Protein; 0/oncogene protein E7, Human papillomavirus type 6

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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