Strain description
In 1997, The Jackson Laboratory imported three strains of SENCAR mice for distribution. The word SENCAR is derived from SENsitivity to CARcinogenesis. An outbred line of these mice has been used extensively for skin carcinogenesis experiments. The late Dr. Michael Potter of the National Cancer Institute developed from the outbred line three inbred lines designated A, B, and C. The fourth strain (SSIN) is being imported from Dr. Claudio Conti at the University of Texas M.D. Anderson Cancer Center.
SENCAR mice are used commonly for experiments with carcinogens and promoter agents to induce carcinogenesis. Although spontaneous neoplasms will occur in older mice, the incidence is low. These spontaneous neoplasms include hematopoietic malignancies, pulmonary adenomas and carcinomas, mammary gland carcinomas and skin neoplasms.
Differences in sensitivity to carcinogens and promotion of progression to squamous cell carcinomas are found among the three lines. A, B, and C lines are all more sensitive to initiation/promotion than the outbred SENCAR strain. Spontaneous papillomas frequently progress to squamous cell carcinomas.
Lines A, B, and C are genetically similar. Line A is the mouse most used and best characterized. SSIN is most used for research on papillomas. The papillomas rarely progress to squamous cell carcinoma prior to one year of age because SSIN mice have lost the progression factor present in SENCAR Lines A, B, and C. SSIN mice are exceptionally sensitive to the promoting actions of several chemical tumor promoters. The H2 haplotype of all four lines is q.
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Line |
Strain Designation |
Stock Number |
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A |
SENCARA/PtJ |
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B |
SENCARB/PtJ |
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C |
SENCARC/PtJ |
Colony maintenance
These strains are inbred and are maintained by mating siblings. The breeding performance is average; however, not all mated pairs will breed well. Breeders are usually retired after two litters. In our experience, no special husbandry requirements are necessary.
References
DiGiovanni, J., Walker, S.C., Beltran, L., Naito, M., Eastin, W.C. Jr. 1991. Evidence for a common genetic pathway controlling susceptibility to mouse skin tumor promotion by diverse classes of promoting agents. Cancer Res 15:1398-1405.
Fischer, S.M., O'Connell, J.F., Conti, C.J., Tacker, K.C., Fries, J.W., Patrick, K.E., Adams, L. M., Slaga, T.J. 1987. Characterization of an inbred strain of the Sencar mouse that is highly sensitive to phorol esters. Carcinogenesis 8:421-424.
Gimenez-Conti, I.B., Bianchi, A.B., Fischer, S.M. Reiners, J.J. Jr., Conti, C.J., Slaga, T.J., 1992. Dissociation of sensitivities to tumor promotion and progression in outbred and inbred Sencar mice. Cancer Res 52:3432-3435.