作者: Marc M. Mareel , Frans M. Van Roy , Patrick De Baetselier
DOI: 10.1007/BF00047588
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摘要: The expression of the invasive (I+ or I-) phenotypes determines cancer metastasis (M+ M- phenotype). can be divided according to time and site into subphenotypes, which assessed separately. At various sites along metastatic pathway I accompanined by presence uncontrolled growth (G+ phenotype) its absence (G- Various combinations G determine behaviour metazoan parasitic cells under normal, pathological non-neoplastic neoplastic conditions. Although G+I+M+ combination correlates with full malignancy, sequence events leading acquisition these during tumor development is not clear. Conditional invasion in experimental systems indicates that a may when part population temporarily expresses I+ phenotype. These experiments further stress importance tumor-host ecosystem for regulation phenotypes. As distinct from some parasites, morphotype vertebrate cannot simply identified. Nevertheless, within morphological activities recognized. They reflect one more functions, namely: motility; loss homotypic cell-cell adhesion; establishment alternative cell-substrate heterotypic breakdown extracellular matrices. functions are exclusive cells, neither molecular markers investigated so far. Oncogene activation leads mainly G+ expression, this way serves as signal amplifier M Attractive candidate are: regulators hydrolase activities; adhesion molecules; cell surface receptors. From data presently available, we hypothesize depends upon balance between an I- pathway, both pathways being sensitive stimulation inhibition.