Neoplastic Conversion In Vitro of Mouse Cells: Cytologic, Chromosomal, Enzymatic, Glycolytic, and Growth Properties

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Abstract
We demonstrated that presumably virus-free cells from the germfree ALBM-2 mouse undergo “spontaneous” neoplastic conversions in vitro. With these cells we showed that a shift from diploidy to heteroploidy is not essential for spontaneous neoplastic conversion in vitro, that the neoplastic cells under the culture conditions used are less adherent to surface substrate than control non-neoplastic cells, and that the growth-pattern change associated with neoplastic conversion may result from a loss of surface-substrate dependency rather than from the hypothetical loss of contact inhibition of mitosis. We extended the serum effect on neoplastic conversion to these presumably virus-free cells. In addition to delaying neoplastic conversion, fetal calf serum (FCS) as compared with horse serum (HS) reduced the percentage of lines converted and increased the latent periods for development of tumors from the cells in vivo. By applying cytologic criteria of neoplastic conversion, we made diagnoses that were 100% consistent with results of in vivo assay. Electron microscope studies showed that the cytoplasmic basophilia in the neoplastic cells was associated with more numerous ribosomes than in non-neoplastic control cells, even when cell populations were increasing at similar rates. As observed earlier, the neoplastic cells increased in glycolytic capacity, with a reduced susceptibility to a glycolytic inhibitor, and had a slightly higher saturation density than non-neoplastic controls, although saturation density increased with time in culture. We extended to embryo cells the observation, made previously on adult and neonatal mouse cells, that alkaline phosphatase activity declines during long-term culture, whereas high acid phosphatase activity is maintained. Changes in arginase activity were not directly related to neoplastic change, but the activity declined in the cells on HS supplement and was maintained in cells on FCS.

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