ReviewCancer metastasis reviews1990
The invasive phenotypes.
Review in Cancer metastasis reviews, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed.
- Mutation or not, what directly establishes a neoplastic state, namely cellular immortality and autonomy, still remains unknown and should be prioritized in our research.Journal of Cancer · 2022Review
- Spontaneous migration of cellular aggregates from giant keratocytes to running spheroids.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Learning about the Importance of Mutation Prevention from Curable Cancers and Benign Tumors.Journal of Cancer · 2016Review
- Distribution and gene mutation of enteric flora carrying β-glucuronidase among patients with colorectal cancer.International journal of clinical and experimental medicine · 2015Article
- c-Myb regulates matrix metalloproteinases 1/9, and cathepsin D: implications for matrix-dependent breast cancer cell invasion and metastasis.Molecular cancer · 2012Article
- Tissue architecture: the ultimate regulator of epithelial function?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 1998Review
- In vitro dynamics of chromatin organization and migration.Cell biology and toxicology · 1996Article
- Quantitative and qualitative differences in growth, invasion and lung colonization of an anaplastic and a papillary human thyroid cancer cell line in vitro and in vivo.Clinical & experimental metastasis · 1996Article
- Morphotypic plasticity in vitro and in nude mice of epithelial mouse mammary cells (NMuMG) displaying an epithelioid (e) or a fibroblastic (f) morphotype in culture.Clinical & experimental metastasis · 1996Article
- Acidic pH enhances the invasive behavior of human melanoma cells.Clinical & experimental metastasis · 1996Article
- The role of fibroblasts in tumor behavior.Cancer metastasis reviews · 1995Review
- In vivo and in vitro invasion in relation to phenotypic characteristics of human colorectal carcinoma cells.British journal of cancer · 1995Article
- Tumour fragment spheroids from human non-small-cell lung cancer maintained in organ culture.Virchows Archiv : an international journal of pathology · 1995Article
- E-cadherin distribution in interleukin 6-induced cell-cell separation of ductal breast carcinoma cells.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- Invasion promoter versus invasion suppressor molecules: the paradigm of E-cadherin.Molecular biology reports · 1994Review
- The p185erbB2 protein is localized on cell organelles involved in cell motility.Clinical & experimental metastasis · 1993Article
- Cyclic AMP distinguishes between two functions of acidic FGF in a rat bladder carcinoma cell line.The Journal of cell biology · 1993Article
- A murine model of intracranial invasion: morphological observations on central nervous system invasion by murine melanoma cells.Clinical & experimental metastasis · 1992Article
- Morphological heterogeneity and phenotypical instability versus metastatic stability in the murine tumor model ER 15-P.Journal of cancer research and clinical oncology · 1992Article
- Cell-cell contacts mediated by E-cadherin (uvomorulin) restrict invasive behavior of L-cells.The Journal of cell biology · 1991Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of the invasive (I+ or I-) phenotypes determines cancer metastasis (M+ or M- phenotype). The invasive (I+ or I-) phenotypes can be divided according to time and site of expression into subphenotypes, which can be assessed separately. At various sites along the metastatic pathway the expression of the I phenotypes can be accompanied by the presence of uncontrolled growth (G+ phenotype) or its absence (G- phenotype). Various combinations of the I and G phenotypes determine the behaviour of metazoan or parasitic cells under normal, pathological non-neoplastic and neoplastic conditions. Although the G+I+M+ combination correlates with full malignancy, the sequence of events leading to the acquisition of these phenotypes during tumor development is not clear. Conditional invasion in experimental systems indicates that a tumor may be invasive and metastatic when part of its population temporarily expresses the I+ phenotype. These experiments further stress the importance of the tumor-host ecosystem for the regulation of the I phenotypes. As distinct from some parasites, the invasive morphotype of vertebrate cells cannot be simply identified. Nevertheless, within the tumor-host ecosystem morphological correlates of the activities of invasive cells may be recognized. They reflect one or more of the I+ functions, namely: motility; loss of homotypic cell-cell adhesion; establishment of alternative cell-substrate and heterotypic cell-cell adhesion; breakdown of extracellular matrices. These functions are not exclusive for I+ tumor cells, and neither are the molecular markers investigated so far. Oncogene activation leads mainly to G+ expression, and in this way serves as a signal amplifier for the I and M phenotypes. Attractive candidate molecular markers of I phenotypes are: regulators of hydrolase activities; cell-cell adhesion molecules; cell surface receptors. From data presently available, we hypothesize that invasion depends upon the balance between and I+ and an I- pathway, with both pathways being sensitive to stimulation inhibition.
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