title: Genetic and epigenetic resistance of SL/Ni mice to lymphomas.
abstract: The murine spontaneous B lymphoma is etiologically related to the expression of endogenous ecotropic murine leukemia virus (ETV). Although both SL/Kh and SL/Ni mouse strains show a high level of expression of ETV from early in life, the former is a pre-B lymphoma-prone strain and the latter is rather lymphoma-resistant. In order to identify the host background difference related to the lymphomagenesis, we performed a genetic cross study between these two strains. In the reciprocal F1 generation, the length of the lymphoma latent period was slightly but significantly longer in (SL/Ni xSL/Kh)F1 than in (SL/KhxSL/Ni)F1(P < 0.05). The incidence of overall lymphomas and that of acute pre-B lymphomas was lower in (SL/NixSL/Kh)F1 than in (SL/KhxSL/Ni)F1, although the difference was not statistically significant. These observations indicate that an epigenetic maternal resistance mechanism of SL/Ni mice plays a role in the lymphoma resistance. Furthermore, in the backcross combinations without maternal influence of SL/Ni, we observed a genetic mechanism of lymphoma resistance: an SL/Ni-derived recessive lymphoma-resistance gene mapped in the proximal segment of Chr. 4. We named this gene nir-1 (SL/Ni-lymphoma resistance-1). Thus, we have demonstrated epigenetic and genetic mechanisms of lymphoma resistance of the SL/Ni mouse with the high expression of endogenous ETV.
authors.affiliation: Laboratory of Pathology, Saitama Cancer Center Research Institute.
authors.forename: H
authors.initials: H
authors.lastname: Shisa
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: A
authors.initials: A
authors.lastname: Kawarai
authors.forename: N
authors.initials: N
authors.lastname: Terada
authors.forename: M
authors.initials: M
authors.lastname: Kawai
authors.forename: H
authors.initials: H
authors.lastname: Matsushiro
authors.forename: H
authors.initials: H
authors.lastname: Hiai
mesh_terms: D000818:Animals; D003433:Crosses, Genetic; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D015967:Gene Expression Regulation, Viral; D005808:Genes, Recessive; D008040:Genetic Linkage; D020022:Genetic Predisposition to Disease; D018392:Genomic Imprinting; D007113:Immunity, Innate / Q000235:genetics; D007112:Immunity, Maternally-Acquired; D009052:Leukemia Virus, Murine / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology; D016393:Lymphoma, B-Cell / Q000235:genetics* / Q000821:virology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics* / Q000821:virology; D018895:Microsatellite Repeats; D008892:Milk / Q000276:immunology; D011533:Proviruses / Q000235:genetics; D013154:Spleen / Q000821:virology; D014779:Virus Replication