Genetic analysis of cell malignancy--evidence from somatic cell genetics.
When normal nontumorigenic cells are fused with tumorigenic cells some of the resulting hybrids are nontumorigenic in respect to their ability to grow in immune-deficient nude mice. Comparison of the chromosome content of nontumorigenic with tumorigenic hybrids, as well as with the cells of tumors which develop from the latter, reveals that in normal human x tumorigenic Chinese hamster hybrid crosses, two specific human chromosomes of the nontumorigenic parental line are very likely responsible for the suppressive effect. In some other hybrid crosses these and additional human chromosomes also seem to cause suppression. These findings suggest that a tumorigenic cell has lost at least two and possibly more gene functions which determine normal growth responses. The chromosomes from a normal cell can apparently correct these defects, although it is not yet clear if this is true genetic complementation or due to introduction of other genes which control cell growth or a cell's response to environmental growth regulatory stimuli. These findings led support to the view that genetic alterations are important in the process of malignant transformation and allow the development of a working hypothesis for the possible mechanisms involved. Some findings of other workers in this area also suggest that malignant cells may be producing some cell membrane proteins which are different from those of nontumorigenic cells. If this turns out to be true then it may ultimately be possible to develop immunotherapeutic procedures, i.e., to produce tumor cell specific antisera.
D000818:Animals; D000912:Antibodies, Neoplasm; D002459:Cell Fusion; D002471:Cell Transformation, Neoplastic; D005809:Genes, Regulator; D006801:Humans; D006822:Hybrid Cells; D007106:Immune Sera; D008565:Membrane Proteins / Q000032:analysis; D051379:Mice; D008819:Mice, Nude
D000912:Antibodies, Neoplasm; D007106:Immune Sera; D008565:Membrane Proteins