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Carcinogenesis Advance Access originally published online on March 14, 2006
Carcinogenesis 2006 27(8):1556-1566; doi:10.1093/carcin/bgl007
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Association of gene expression with sequential proliferation, differentiation and tumor formation in murine skin

Katie Ridd, Shu-Dong Zhang, Richard E. Edwards, Reginald Davies, Peter Greaves, Alison Wolfreys1, Andrew G. Smith and Timothy W. Gant*

MRC Toxicology Unit Hodgkin Building, Lancaster Road, PO BOX 138 University of Leicester Leicester, LE1 9HN, UK
1 Safety and Environmental Assurance Centre, Unilever Colworth, Sharnbrook, Bedfordshire, MK44 1LQ, UK

*To whom correspondence should be addressed: Tel: +0116 252 5579; Fax: +0116 252 5616; Email: twg1{at}le.ac.uk

Differential gene expression in two established initiation and promotion skin carcinogenesis models during promotion and tumor formation was determined by microarray technology with the purpose of distinguishing the genes more associated with neoplastic transformation from those linked with proliferation and differentiation. The first model utilized dimethylbenz[a]anthracene initiation and 12-O-tetradecanoylphorbol 13-acetate (TPA) promotion in the FVB/N mouse, and the second TPA promotion of the Tg.Ac mouse, which is endogenously initiated by virtue of an activated Ha-ras transgene. Comparison of gene expression profiles across the two models identified genes whose altered expression was associated with papilloma formation rather than TPA-induced proliferation and differentiation. DMBA suppressed TPA-induced differentiation which allowed identification of those genes associated more specifically with differentiation rather than proliferation. EASE (Expression Analysis Systemic Explorer) indicated a correlation between muscle-associated genes and skin differentiation, whereas genes involved with protein biosynthesis were strongly correlated with proliferation. For verification the altered expression of selected genes were confirmed by RT–PCR; Carbonic anhydrase 2, Thioredoxin 1 and Glutathione S-transferase omega 1 associated with papilloma formation and Enolase 3, Cystatin ß and Filaggrin associated with TPA-induced proliferation and differentiation. In situ analysis located the papillomas Glutathione S-transferase omega 1 expression to the proliferating areas of the papillomas. Thus we have identified profiles of differential gene expression associated with the tumorigenesis and promotion stages for skin carcinogenesis in the mouse.


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