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Publication : Genetic and epigenetic resistance of SL/Ni mice to lymphomas.

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.
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