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THE INFLUENCE OF GENETIC VARIABILITY OF TUMOR CELL POPULATION OF MOUSE HEPATOMA MH-22a ON INTERINDUCTION OF APOPTOSIS BETWEEN TUMOR HEPATOCYTES AND SPLENOCYTES
Heterogeneity of tumors by different features increases during tumor progression and determines the level of its malignancy. To reveal possible correlations between different characteristics, the method of clonal analysis of the tumor cell population should be used. The goal of this study was to reveal the influence of DNA-polymorphism level of mouse hepatoma cells MH-22a on their abilities to differentiate upon the growth in the eye anterior chamber (EAC), to induce apoptosis of splenocytes at cocultivation, and to resist to splenocyte-induced apoptosis. The DNA-polymorphism was revealed using RAPD-PCR with three random primers. The ability of tumor hepatocytes for differentiation was determined by transplantation into the EAC of syngenic mice C3HA. The capability for apoptosis interinduction between tumor hepatocytes and syngenic splenocytes was determined upon cocultivation in vitro with the use of electrophoresis of low molecular DNA fractions and by the method of clonal survival. It was shown that the clonal lines MH-22a with a high level of genetic variability were unable to differentiate if they are grown in EAC, were stable to apoptosis induction by splenocytes, but could induce apoptosis in splenocytes. The basic population of tumor hepatocytes and clonal lines characterized by low level of genetic variability differentiated during the growth in EAC and had capability for interinduction of apoptosis with syngenic splenocytes.
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