SENCAR mouse skin tumorigenesis model versus other strains and stocks of mice.

Abstract

The SENCAR mouse stock was selectively bred for eight generations for sensitivity to skin tumor induction by the two-stage tumorigenesis protocol using 7,12-dimethylbenz(a)anthracene (DMBA) as the initiator and 12-0-tetradecanoylphorbol-13-acetate (TPA) as the promoter. The SENCAR mouse was derived by crossing Charles River CD-1 mice with skin-tumor-sensitive mice (STS). The SENCAR mice are much more sensitive to both DMBA tumor initiation and TPA tumor promotion than CD-1, BALB/c, and DBA/2 mice. An even greater difference in the sensitivity to two-stage skin tumorigenesis is apparent between SENCAR and C57BL/6 mice when using DMBA-TPA treatment. However, the SENCAR and C57BL/6 mice have a similar tumor response to DMBA-benzoyl peroxide treatment, suggesting that TPA is not an effective promoter in C57BL/6 mice. The DBA/2 mice respond in a similar manner to the SENCAR mice when using N-methyl-N-nitro-N-nitrosoguanidine (MNNG)-TPA treatment. The SENCAR mouse model provides a good dose-response relationship for many carcinogens used as tumor initiators and for many compounds used as tumor promoter. When compared to other stocks and strains of mice, the SENCAR mouse has one of the largest data bases for carcinogens and promoters.

Development of Keratoacanthomas and Squamous Cell Carcinomas in Transgenic Rabbits with Targeted Expression of EJras. Oncogene in Epidermis

“…6 These results clearly indicate the involvement of activated Ha-ras genes in the development of both benign and malignant skin tumors. The roles of activated Ha-ras in skin tumor development are further supported by animal studies, including carcinogen-treated animals [7][8][9][10][11] and transgenic animals. [12][13][14][15][16][17] Mouse skin carcinogenesis as a biological model has been used to study Ha-ras activation-related skin tumors for many years.…”

“…The Sencar mice are the most widely used model for studying so-called two-stage carcinogenesis because of their sensitivity to the carcinogens 7, 12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). 8 At the molecular level, mutation of Ha-ras (A-to-T transversion) in codon 61 has been identified as one initiating event in skin tumors by the carcinogens, most notably DMBA. 7,9,11 Similar results have also been obtained from studies of DMBA-treated rabbits.…”

Advanced Glycation Endproducts Act as An Initiator of Skin Tumors in Mice

“…genesis initiated by DMBA and promoted by TPA [13]. Skin tumors formed on mice initiated with DMBA and 100 µg of AGEs-BSA, whereas no tumors formed on mice initiated with either low dose AGEs-BSA (10 µg) or unmodified BSA.…”

Effect of Sodium Arsenite on Mouse Skin Carcinogenesis

“…Female SENCAR mice aged 7 to 9 weeks (Slaga 1986) were used for the experimental protocols described in the subsequent text. The animals were bred at the Argentine Atomic Energy Commission and housed with environmentally controlled temperature and humidity and a 12-hr light/dark cycle.…”