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Results for “SARCOMA, YOSHIDA”

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At least 19 recordsLinked to original sources
PubMed1980

DNA synthesis in tumor-bearing rats: purification of liver thymidine kinase stimulating factor from Yoshida sarcoma.

Yoshida sarcoma cells contain a factor that stimulates thymidine kinase activity in the liver of mice in vivo; intraperitoneal injection of an extract from Yoshida sarcoma into normal mice stimulated their liver thymidine kinase activity 2- to 3-fold, whereas injection of a crude extract of normal rat liver did not stimulate the activity at all. A factor that stimulates the de novo synthesis of thymidine kinase in the liver was partially purified from Yoshida sarcoma by ammonium sulfate fractionation, DEAE-cellulose column chromatography and gel filtration. It appeared to be thermolabile and sensitive to trypsin treatment. These results suggested that it was a high-molecular weight protein. Intraperitoneal injection of this factor into 67% hepatectomized rats stimulated thymidine kinase activity 2- to 3-fold. Increase of liver thymidine kinase activity after injection of the factor into mice was blocked by simultaneous injection of actinomycin-D. These results suggest that this factor stimulates de novo synthesis of thymidine kinase in the liver.

Animals↗
PubMed1994

Isolation of genes differentially expressed between the Yoshida sarcoma and long-survival Yoshida sarcoma variants: origin of Yoshida sarcoma revisited.

The Yoshida sarcoma (YS) is characterized by growth as "free cells" in ascites. Long-survival Yoshida sarcoma (LY) variants, which develop after transplantation of YS into immunologically conditioned Donryu rats, in contrast, form "islands" in ascites. A representational difference analysis (RDA) approach was adopted to isolate genes differentially expressed between YS and LY variants to elucidate the molecular mechanism of their development. Fifteen clones presenting differences in expression were characterized. Nine genes (those encoding for the high-affinity IgE receptor gamma chain, pJG116 repetitive sequence, non neuronal enolase, proteasome subunit RC1, cytotoxic T lymphocyte-associated gene transcript CTLA-1, interleukin-2 receptor gamma chain, and three unknown sequences) expressed mRNA in YS, but showed lower or no expression of mRNA in LYs. The mRNAs of the other six genes (those encoding for cytokeratin 8, cytokeratin18 (Endo B), TIMP2 and three unknown sequences) were not found in YS, but were present in LYs. Interestingly, CTLA-1 is a non-epithelial (hematopoietic) cell-specific gene in terms of transcription, while cytokeratin 8 and cytokeratin 18 are both epithelium-specific genes. Immunohistochemically, YS expressed T-cell specific antigens CD2 and CD3, and T cell receptor beta and gamma chain genes were rearranged in YS, but not in LYs. Moreover, using restriction fragment length polymorphism probes, we found that LYs exhibited different cell lineage from YS. Thus, our present findings, unexpectedly, raise fundamental questions concerning the cellular origins of YS and LY variants rather than pointing to any specific mechanism to explain the LY phenomenon.

Animals↗
PubMed1982

Radiation effect on partially synchronized Yoshida sarcoma cells.

Yoshida sarcoma cells, which have the same growth characteristics as ascites cells in the mouse and in cell suspension, were partially synchronized in vitro by means of excess thymidine (0.1 mM thymidine for 18 h). The growth of non-synchronized cultures was inhibited by irradiation, the degree depending on the dose of radiation. At the same time, a 50% inhibition in vivo (380 rad) and in vitro (480 rad) was determined. The incorporation of 3H-thymidine into the DNA is inhibited by 10-32%, depending on the radiation dose. The mitotic index decreases 2 h after irradiation by a dose-dependent amount. A mitotic maximum develops later; the delay is dose-dependent. Partially synchronized cells were irradiated in the G1/S-, G2-, and G1-phase. As compared to the 3H-thymidine incorporation and the mitotic index there were no significant differences between the cultures which were irradiated in the individual phases of the non-synchronized control cultures. The cultures which were irradiated in the G2-phase, however, showed a significantly reduced growth in vivo after 48 h. If the cells were cultured for more than 72 h after irradiation, the differences between the cultures irradiated in the G2-phase and the other phases were reduced.

Animals↗