Abstract
Tumor progression from low to high malignancy is believed to occur in multiple steps (1). Analogous to mutation/selection the process of tumor progression is thought to have its basis in the continuous emergence of successive clones of tumor cell variants, one gradually replacing another, through the intervention of natural or artificial selection pressures (2). Highly malignant metastasizing tumor cells have been shown to differ from low malignant non-metastasizing ones in a number of properties such as plasma membrane enzyme activities (3), cell surface antigen shedding (4), tumor antigenicity and immunogenicity (5). A critical question is whether all these specific properties have been accumulated in the metastatic cell in a stepwise fashion. Is each new property the result of a process of random variation and host selection? How can a random process result in the generation of cells endowed with not just one but a number of very specific properties that enable them to cross the various biological barriers of the host, to survive and grow in different microenvironments?
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References
P. C. Nowell, The clonal evolution of tumor cell populations, Science 194: 23 (1976).
R. S. Kerbel, Implications of immunological heterogeneity of tumours, Nature 280: 358 (1979).
S. K. Chatterjee, U. Kim and K. Bielot, Plasma membrane associated enzymes of mammary tumors as the biochemical indicators of metastasizing capacity. Analyses of enriched membrane fragments, Brit.J.Cancer 33: 15 (1976).
P. Alexander, Escape from immune destruction by the host through shedding of membrane antigens: is this a characteristic shared by malignant and embryonic cells? Cancer Res. 34: 2077 (1974).
E. V. Sugarbaker and A. M. Cohen, Altered antigenicity in spontaneous pulmonary metastases from an antigenic murine sarcoma, Surgery 72: 155 (1972).
G. T. Diamandopoulos, Microenvironmental influences on the in vivo behavior of neoplastic lymphocytes, Proc.Nat.Acad.Sci. 76: 6456 (1979).
D. Brouty-Boye, I. Gresser and C. Baldwin, Reversion of the transformed phenotype to the parental phenotype by subcultivation of x-ray transformed C3H/10 T 1/2 cells at low cell density, Int.J.Cancer 24: 253 (1979).
D. Brouty-Boye and I. Gresser, Reversibility of the transformed and neoplastic phenotype. I. Progressive reversion of the phenotype of X-ray transformed C3H/10 T 1/2 cells under pro-longed treatment with interferon, Int.J.Cancer 28: 165 (1981).
B. Minz and K. Illmensee, Normal genetically mosaic mice produced from malignant teratocarcinoma cells, Proc.Nat.Acad.Sci. 72: 3585 (1975).
I. Parr, Response of syngeneic murine lymphomata to immunotherapy in relation to the antigenicity of the tumor, Brit.J.Cancer 26: 174 (1972).
V. Schirrmacher, G. Shantz, K. Clauer, D. Komitowski, H.-P. Zimmermann, M. L. Lohmann-Matthes, Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. I. Tumor invasiveness in vitro and metastases formation in vivo, Int.J.Cancer 23: 233 (1979).
P. Altevogt, J. T. Kurnick, A. K. Kimura, K. Bosslet and V. Schirrmacher, Different expression of Lyt differentiation antigens and cell surface glycoproteins by a murine T lymphoma line and its high metastatic variant, Eur. J. Immunol. (in press 1981).
M.-L. Lohmann-Matthes, A. Schleich, G. Shantz and V. Schirrmacher, Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. VII. Interaction of metastasizing and non-metastasizing tumors with normal tissue in vitro, J.Natl. Cancer Inst. 64: 1413 (1980)
V. Schirrmacher, R. Cheingsong-Popov, and H. Arnheiter, Hepatocyte-tumor cell interaction in vitro. I. Conditions for rosette formation and inhibition by anti H-2 antibody, J.Exp.Med. 151: 984 (1980).
V. Schirrmacher and W. Jacobs, Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. VIII. Expression and shedding of Fc receptors on metastatic tumor cell variants, J.Supramol.Struct. 11: 105 (1979).
V. Schirrmacher, K. Bosslet, G. Shantz, K. Clauer and D. Hiibsch, Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. IV. Antigenic differences between the parental tumor line and its metastasizing variant, Int.J.Cancer 23: 245 (1979).
K. Bosslet, V. Schirrmacher, and G. Shantz, Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. VI. Similar specificity patterns of protective anti-tumor immunity in vivo and of cytolytic T cells in vitro, Int.J.Cancer 24: 303 (1979).
V. Schirrmacher and K. Bosslet, Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. X. Immuno-selection of tumor variants differing in tumor antigen expression and metastatic capacity, Int. J. Cancer 25: 781 (1980).
V. Schirrmacher, D. Hiibsch and K. Clauer, Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. IX. Radioassay analysis of tumor cell spread from a local site to the blood and liver, in: “Metastatic Tumor Growth, Cancer Campaign,” E. Grundmann, ed., Gustav Fischer Verlag 4: 147 (1980).
D. Barz, K. Bosslet and V. Schirrmacher, Metastatic tumor cell variants with increased resistance to infection by Semliki Forest Virus, J.Immunology 127: 951 (1981).
V. Schirrmacher, Shifts in tumor cell phenotypes induced by signals from the microenvironment: Relevance for the immune-biology of cancer metastasis, Immunobiology 157: 89 (1980).
K. Bosslet and V. Schirrmacher, Escape of metastasizing clonal tumor cell variants from tumor-specific cytolytic T lymphocytes, J.Exp.Med. 154: 557 (1981).
G. Poste and I. J. Fidler, The pathogenesis of cancer metastasis, Nature 283: 139 (1980).
I. J. Fidler and M. L. Kripke, Metastasis results from preexisting variant cells within a malignant tumor, Science 197: 893 (1977).
G. I. Nicolson, Cancer Metastasis, Scientific America 240: 50 (1979).
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Schirrmacher, V., Altevogt, P., Bosslet, K. (1983). Spontaneous Phenotypic Shifts from Low to High Metastatic Capacity. In: Chandra, P. (eds) Biochemical and Biological Markers of Neoplastic Transformation. NATO Advanced Science Institutes Series, vol 57. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4454-4_10
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DOI: https://doi.org/10.1007/978-1-4684-4454-4_10
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