SL

Inbr(A) ?+90. Albino: A,B,c. Origin: Outbred Swiss mice to Keio University in 1941, University of Tokyo in 1944, then Hokkaido University at an unknown date and Misima in 1951. Derived as a high-leukaemia strain by K. Tsuchikawa in Misima. Transferred to Kyushu University in 1954 from where the four current substrains are derived. These differ in leukaemia incidence, ecotropic virus expression, as well as for a number of genetic markers (Hiai et al 1987). A detailed genetic analysis of the four substrains designated SL/QDj, SL/Am, SL/Ni and SL/Kh using 100 microsatellite markers showed that the Am and Ni substrains were almost identical, though they differ in biological characteristics with the Am strain having a high incidence of lymphoma not found in the Ni substrain. SL/Kh has probably been contaminated by AKR, and the QDj substrain seems to be a recombinant between the Am and Kh substrains. All four substrains have the H2^q haplotype. The Ni and Am substrains carry the type 1 Mx gene conferring resistance to influenza virus, also found in strain A2G (Abujiang et al, 1996).

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Characteristics

In Misima leukaemia incidence is low (Tajima, 1968). Kh substrain develops B-lymphomas associated with a gene in the H2 complex (Yamada et al, 1994), and ecotrophic murine leukemia viruses (Pataer et al, 1996). High and early incidence of nonthymic lymphomas at an unusually early age, with a cumulative incidence of 88% in females and 48% in males by the age of six months, rising to 100% in females and 94% in males by 12 months. Two types of poorly differentiated leukemias were seen with the major type proliferating in lymph nodes and the spleen and the minor type in the bone marrow, causing paraplegia by spinal compression with many host and epigenetic factors favourable for lymphoma development (Hiai, 1996). Other papers describing SL/Kh include Hial et al, (1992), Shimada et al, (1993) and Lu et al, (1997).

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Abujiang P., Yamada Y., Haller O., Kobayashi H., Kamoto T., Lu L. M., Ogawa M., Ishimoto A., Katoh H., Kanehira K., Ikegami S., Fukumoto M., and Hiai H. (1996) The origin of SL family mice. Lab. Animal Sci. 46, 410-417.

Hiai H., Buma Y. O., Ikeda H., Moriwaki K., and Nishizuka Y. (1987) Epigenetic control of endogenous ecotropic virus expression in SL/No mice. J. Natl. Cancer Inst. 79, 781-787.

Hiai H. (1996) Genetic predisposition to lymphomas in mice. Pathology International 46, 707-718.

Lu L.-M., Ogawa M., Kamoto T., Yamada Y., Abujiang P., and Hiai H. (1997) Expression of LECAM-1 and LFA-1 on pre-B lymphomaz cells but not on preneoplastic pre-B cells in SL/Kh mice. Leuk. Res. 21, 337-342.

Pataer A., Kamoto T., Lu L. M., Yamada Y., and Hiai H. (1996) Two dominant host-resistance genes to pre-B lymphoma in wild-derived inbred mouse strain MSM/Ms. Cancer Res. 56, 3716-3720.

Shimada A., Ohta A., Akiguchi I., and Takeda T. (1993) Age-related deterioration in condition avoidance taks in the SAM-P/10 mouse, an animal model for spontaneous brain atrophy. Brain Res. 608, 266-272.

Tajima Y. (1968) Stansardized nomenclature for inbred strains of mice. Experimental animals in cancer research. Japanese Cancer Association Gann Monograph 5, 123-128.

Yamada Y., Shisa H., Matsushiro H., Kamoto T., Kobayashi Y., Kawarai A., and Hiai H. (1994) T lymphomagenesis is determined by a dominant host gene thymic lymphoma susceptible mouse-1 (Tlsm-1) in mouse models. Journal Of Experimental Medicine 180, 2155-2162.

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INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK