Kobe Journal of Medical Sciences, 1991
TI: Possible collaboration between c-fos and c-myc proto-oncogene products in in vivo lymphomagenesis.
AU: Takao-S; Sakai-N; Aizawa-S; Tokuhisa-T
AD: Department of Immunology, ICMR, Kobe University School of Medicine, Japan.
SO: Kobe-J-Med-Sci. 1991 Oct; 37(4-5): 227-43
AB: Transgenic mice carrying the exogenous c-myc gene under regulation of the Ig enhancer (Ig-c-myc) were mated with mice carrying exogenous c-fos gene under control of the H-2Kb promoter (H2-c-fos) to examine their functional collaboration in in vivo lymphomagenesis. Two of the 33 (c-fos x c-myc) mice developed pre-B cell lymphomas within 22 weeks of age. None of the other F1 progeny expressing c-fos or c-myc alone showed malignant change within 14 months of age, suggesting that the exogenous c-fos and c-myc collaborate in in vivo lymphomagenesis. The exogenous c-myc RNA was overexpressed in the lymphomas, but the amount of exogenous c-fos RNA was not affected, suggesting that the large abundance of c-myc protein is a prerequisite for lymphoma onset or progression and c-fos protein plays a complementary role. C-fos protein induced immunodeficiency in the (c-fos x c-myc) mice like H2-c-fos mice. Natural killer cell activity of (c-fos x c-myc) mice was partially impaired. Therefore, these lymphomas may be a consequence of the synergism of two independent actions caused by the exogenous c-myc (lymphomagenesis) and the exogenous c-fos (low NK activity) in (c-fos x c-myc) mice.