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  • Title: Tumor cell hybridization and neoplastic progression.
    Author: Hart IR.
    Journal: Symp Fundam Cancer Res; 1983; 36():133-43. PubMed ID: 6382503.
    Abstract:
    In the experiments reported here, I was unable to detect any fusion between host cells and transplanted tumor cells; however, spontaneous hybridization between tumor cells appears to occur in the B16 melanoma. This hybridization was demonstrated by mixing together B16-F10RR cells (universal fusers) and B16-F10 cells, allowing them to grow in close juxtaposition, and recovering putative hybrids in the appropriate selection media. The tumor cell-tumor cell composition of the resultant hybrids is inferred from the relative frequency of fusions, compared with the infrequency of tumor cell-host cell fusion when single populations of B16-F10RR cells were used, and by the chromosomal content of the hybrids. Definitive proof that hybridization occurs between both types of tumor cell rather than between a tumor cell and some other type of cell would require the use of a third biochemical marker on the unmarked tumor cells. I am now repeating these experiments using B16-F10 cells that exhibit resistance to the neomycinlike antibiotic G418. Nonetheless, it is not surprising to find that such closely related tumor cells fuse with one another. The efficiency of in vitro hybridization mediated by polyethylene glycol is increased when the hybridizing cells are histologically or developmentally related, so that B16 melanoma cells fuse more readily with one another than they do with unrelated cells such as UV-2237 cells (I. Hart, unpublished observations). Moreover, early hybridization protocols did not call for the use of fusogens, but merely the cocultivation of participating cells in the two-dimensional constraints of a tissue culture dish (e.g., Barski et al. 1961, Silagi 1967). Presumably, the increased contact between cells within a growing tumor mass would increase the likelihood of such spontaneous fusion. In vivo hybridization could play a significant role in neoplastic progression and variation in metastatic efficiency by at least two separate, but not necessarily mutually exclusive, mechanisms. First, fusion of two contiguous tumor cells would increase the chromosome content of the resultant single cell; this increase in ploidy could facilitate and heighten the apparent inherent genetic instability of neoplastic cells (Nowell 1976). Although segregation and chromosome loss may or may not be random or preferential in nature (Campbell and Worton 1981), the mere occurrence of such a phenomenon could also cause chromosomal disjunction and the possible extinction and reexpression of specific genes, which would lead to the independent variation and progression of different tumor cell characteristics in the manner cited by Foulds (1969).(ABSTRACT TRUNCATED AT 400 WORDS)
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