First Author | Shisa H | Year | 1996 |
Journal | Jpn J Cancer Res | Volume | 87 |
Issue | 3 | Pages | 258-62 |
PubMed ID | 8613427 | Mgi Jnum | J:32436 |
Mgi Id | MGI:79932 | Doi | 10.1111/j.1349-7006.1996.tb00214.x |
Citation | Shisa H, et al. (1996) Genetic and epigenetic resistance of SL/Ni mice to lymphomas. Jpn J Cancer Res 87(3):258-62 |
abstractText | 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 F-1 generation, the length of the lymphoma latent period was slightly but significantly longer in (SL/Ni X SL/Kh)F-1 than in (SL/Kh X SL/Ni)F-1 (P < 0.05), The incidence of overall lymphomas and that of acute pre-B lymphomas was lower in (SL/Ni X SL/Kh)F-1 than in (SL/Kh X SL/Ni)F-1, 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. |