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Publication : The possible mechanism of enhanced carcinogenesis induced by genotoxic carcinogens in rasH2 mice.

First Author  Okamura M Year  2007
Journal  Cancer Lett Volume  245
Issue  1-2 Pages  321-30
PubMed ID  16530936 Mgi Jnum  J:117163
Mgi Id  MGI:3695766 Doi  10.1016/j.canlet.2006.01.025
Citation  Okamura M, et al. (2007) The possible mechanism of enhanced carcinogenesis induced by genotoxic carcinogens in rasH2 mice. Cancer Lett 245(1-2):321-30
abstractText  Microarray and RT-PCR analyses were performed for the transgene and Ras-related genes in forestomach squamous cell carcinomas (SCCs) induced by 7,12-dimethylbenz[a]anthracene (DMBA) in rasH2 mice; these results were compared with our previous molecular data of N-ethyl-N-nitrosourea-induced forestomach SCCs and urethane-induced lung adenomas in rasH2 mice. Overexpression of the transgene was detected in the DMBA-induced SCCs, suggesting that the transgene plays an important role in enhanced carcinogenesis in rasH2 mice. In addition, the mouse endogenous ras genes were up-regulated in the DMBA-induced SCCs, and are probably involved in the tumorigenesis of forestomach SCCs. Genes such as osteopontin, Cks1b, Tpm1, Reck, gelsolin, and amphiregulin that were commonly altered in these three different carcinogen-induced tumors may contribute to the development of tumors in rasH2 mice.
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