Susceptibility loci and chromosomal abnormalities in radiation induced hematopoietic neoplasms in mice.

Genetics of susceptibility to radiation-induced hematopoietic neoplasms and somatic chromosomal aberrations were analyzed in 305 backcross (CcS-17xCcS-2)xCcS-2 mice of two CcS/Dem recombinant congenic strains. Irradiated CcS-2 mice were previously shown to exhibit high frequency of myeloid neoplasms whereas irradiated CcS-17 mice were susceptible to T-cell lymphomas. Mice were exposed to four whole-body irradiation doses of 1.

Opposite effects of modifiers of the ApcMin mutation in intestine and mammary gland.

Patterns of tumor susceptibility in different organs are widely divergent in mouse strains: one strain may be highly susceptible to tumors in one organ but resistant in another organ, whereas another strain may exhibit the opposite pattern (P. Demant, Semin. Cancer Biol.

Genetics of susceptibility to radiation-induced lymphomas, leukemias and lung tumors studied in recombinant congenic strains.

The genetic control of susceptibility to radiation-induced tumors in mice has been tested using the series of 20 CcS/Dem (CcS) Recombinant Congenic Strains, each carrying a different random set of 12.5% of genes of the resistant strain STS/A (STS) on the genetic background of the susceptible strain BALB/cHeA (BALB/c). Two classes of tumors were frequently observed: tumors of the haematopoietic system (lymphomas, myelocytic leukemias) and lung tumors.

Effects of thiol compounds on methotrexate uptake by murine lymphocytes from thymus and thymic lymphosarcoma.

The characteristics of methotrexate (MTX) uptake and the effects of exogenous sulfhydryl compounds (i.e. reduced glutathione and cysteine) on MTX accumulation in thymocytes and thymic lymphosarcoma cells has been studied.

Effects of riboflavin on benzo(a)pyrene, 2-acetylaminofluorene and methyl methanesulfonate mutagenicity in vitro.

Riboflavin was shown to inhibit mutagenicity of benzo(a)pyrene and 2-acetylaminofluorene in the presence of S9 liver fractions deriving from B10.A mice as well as from DBA/2 mice and had no influence on mutagenicity of methyl methanesulfonate. The above findings confirm the supposition that antimutagenicity of riboflavin results from its interaction with enzymes responsible for metabolic activation of promutagens.