SENCAR mouse

KATiYAR s K and MUKHTAR H (1997) Inhibition of phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate-caused inflammatory responses in SENCAR mouse skin by black tea polyphenols . Carcinogenesis, 18 1911-16. 

J. P., et al. (1997) Evidence that initiated ker-atinocytes clonally expand into multiple existing hair follicles during papilloma histogenesis in SENCAR mouse skin. Mol CarcinoglO, 151-158. 

Hennings, H., Blumberg, P. M., Pettit, G. R., Herald, C. L., Shores, R., and Yuspa, S. H., Bryostatin 1, an activator of protein kinase C, inhibits tumor promotion by phorbol esters in SENCAR mouse skin, Carcinogenesis, 8, 1343, 1987. 

D. Chakravarti, P. C. Mailander, K.-M. Li, S. Higginbotham, and H. L. Zhang, Evidence that a burst of DNA depurination in SENCAR mouse skin induces error-prone repair and forms mutations in the H-ras gene. Oncogene 20 (2001), 7945-7953. 

SENCAR mouse skin tumorigenesis bioassay system, OKNL/TM-9752, AD-A159 728, Oak Ridge... 

Chakravarti, D., Mailander, R, Franzen, J., Higginbodiam, S., Cavalieri, E. L., and Rogan, E. G. (1998). Detection of dibenzo[a,/]pyrene-induced H-ras codon 61 mutant genes in preneoplastic SENCAR mouse skin using a new RCR-RFLR method. Oncogene 16, 3203-3210. 

Vulimiri, S. V., Baer-Dubowska, W., Harvey, R. G., Zhang, J. T, and DiGiovanni, J. (1999). Analysis of highly polar DNA adducts formed in SENCAR mouse epidermis following topical appUcation of dibenzfajjanthracene. Chem Res Toxicol 12, 60-67. 

DNA was capable of malignantly transforming NIH 3T3 cells in DNA transfection studies (411). Studies in our laboratory (41) indicate that initiation alone or repetitive TPA treatments are insufficient to turn on the expression of the Ha-raa oncogene in adult SENCAR mouse epidermis. Initiation followed by either one or six weeks of TPA treatment also failed to activate Ha- ga expression. Like Balmain, we observed elevated levels of Ha-ras RNA in a percentage of papillomas and carcinomas tested. We have also found that the expression of c-sis. and c-aU are increased in the majority of carcinomas examined (42). It remains to be determined whether oncogene activation plays a critical role in multistage skin carcinogenesis. 

Klann RC, Fitzgerald D J, Piccoh C, Slaga TJ, Yamasaki H. Gap-junctional intercellular communication in epidermal cell hues from selected stages of SENCAR mouse skin carcinogenesis. Cancer Res i989 49 699-705. 

Chen, L.C., Sly, L., Jones, C.S., Tarone, R., and De Luca, L.M., Differential effects of dietary beta-carotene on papilloma and carcinoma formation induced by an initiation-promotion protocol in SENCAR mouse skin. Carcinogenesis, 14, 713,1993. 

Katiyar, S.K., Agarwal, R., Wang, Z. Y., Bhatia, A.K., and Mukhtar, H., (-)-Epigallocatechin-3-gallate in Camellia sinensis leaves from Himalayan region of Sikkim inhibitory effects against biochemical events and tumor initiation in SENCAR mouse skin, Nutr. Cancer, 18, 73-83, 1992b. 

We are aware too that genetics can play a role in susceptibility. Should one therefore select a sensitive animal model or a resistant one For example, for skin carcinogenesis, the SENCAR mouse is regarded as extremely sensitive to many carcinogens, in particular polycyclic aromatic hydrocarbons. On the other hand, C57 Black mice are insensitive to benzopyrene as an initiator. 

Zhao J, Lahiri-Chatteijee M, Sharma Y, Agarwal R. Inhibitory effect of a flavonoid antioxidant silymarin on benzoyl peroxide-induced tumor promotion, oxidative stress and inflammatory responses in SENCAR mouse skin. Carcinogenesis 2000 21(4) 811-816. 

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