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Virus-induced leukemia was inoculated into histocompatible or allogeneic hosts pretreated with 5-(3,3'-dimethyl-1-triazeno)-imidazole-4-carboxamide (DTIC) + Cyclophosphamide (Cy), which abrogate endogenous cell proliferation and T-dependent graft responses, but not selected "natural resistance" (NR) activities. Marked impairment of lymphoma cell growth occurred mainly in the spleen of allogeneic mice with respect to that of histocompatible controls. Tumor inhibition was still present when lymphoma challenge was performed on day + 3 after Cy administration. Parallel studies on "natural killer" (NK) activity in vitro or in vivo showed that complete abrogation of the NK function was detectable on day + 3 or + 6 after Cy treatment. It was concluded that in vivo inhibition of lymphoma growth in mice pretreated with DTIC + Cy could be a drug-resistant NR at least in part distinguishable from the NK function.
F Campanile, and
A M Iorio, and
E Bonmassar
January 1978,
Journal of immunopharmacology,
F Campanile, and
A M Iorio, and
E Bonmassar
September 1980,
Cancer letters,
F Campanile, and
A M Iorio, and
E Bonmassar
September 1979,
Cancer,
F Campanile, and
A M Iorio, and
E Bonmassar
June 1977,
Biochemical and biophysical research communications,
F Campanile, and
A M Iorio, and
E Bonmassar
December 1984,
Journal of medicinal chemistry,
F Campanile, and
A M Iorio, and
E Bonmassar
July 1979,
European journal of cancer,
F Campanile, and
A M Iorio, and
E Bonmassar
January 1982,
Carcinogenesis,
F Campanile, and
A M Iorio, and
E Bonmassar
October 1972,
Cancer chemotherapy reports,
F Campanile, and
A M Iorio, and
E Bonmassar
October 1986,
Biochemical pharmacology,
F Campanile, and
A M Iorio, and
E Bonmassar
December 1981,
Cancer research,
