Increased tumorigenicity of polyploid Ehrlich variants during growth in vivo is associated with karyotypic changes.
In previous studies, treatment of Ehrlich ascites tumors (EAT) with either Sendai virus, Herpes virus or neuraminidase produced variants that differed significantly from EAT in both tumorigenicity and karyotype. In this study, less tumorigenicity variants of EAT were isolated by culturing in media containing low concentrations of serum or without serum. In contrast to the relative stability of tumorigenicity in such variants cultured in vivo, the tumorigenicity of these variant clones passaged in vivo was variable, depending on the variant clone. During growth in vivo, 3 variant clones independently isolated from serum-free medium, low serum-containing medium and after neuraminidase treatment produced markedly heterogeneous tumors, and after 4 passages the tumors were about 1000 times more tumorigenic than the initial variants. In generating new tumors, the tumors always segregated chromosomes. The banded chromosome analysis of a variant clone isolated from serum-free medium and its malignant tumor showed that most of the chromosomes segregated from the clone were normal types. On the other hand, the tumorigenicity of Herpes virus-induced variants was unchanged during growth in vivo.
D000818:Animals; D002286:Carcinoma, Ehrlich Tumor / Q000235:genetics* / Q000473:pathology; D002999:Clone Cells; D003470:Culture Media; D014644:Genetic Variation; D007621:Karyotyping; D051379:Mice; D009368:Neoplasm Transplantation
D003470:Culture Media