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The Evolution of Phenotypic Diversity in Metastatic Tumor Cells

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Biological Responses in Cancer

Abstract

It has been approximately one hundred years since Paget (1889) proposed the “seed and soil” hypothesis of tumor spread. This hypothesis was developed to explain the nonrandom occurrence of metastases in particular organs. Paget proposed that the microenvironment in unique organs or tissues (“soil”) influenced the extravasation, survival, and growth of particular tumor cells (“seeds”). This hypothesis has remained one of the most important concepts of tumor metastasis. We now know that malignant neoplasms are composed of diverse cell “seeds” that are heterogeneous for a multitude of cellular properties, including cellular morphology, surface antigens, glycolipids, glycoproteins, recognition and adhesion components, and degradative and biosynthetic enzymes. They are also quite variable in their abilities to communicate with other cells, invasiveness, and metastatic properties, and, as expected, heterogeneity also exists in their sensitivities to various therapeutic agents (such as drugs, radiation, and hyperthermia), as well as host—response mechanisms (reviewed in Hart and Fidler, 1981; Fidler and Hart, 1982; Nicolson, 1982, 1984a; Nicolson and Poste, 1982, 1983a,b). Heterogeneity in cellular properties is also present in normal cells and tissues, but the range of diversity may not be as extensive as in malignant neoplasms (Peterson et al., 1981, 1983).

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© 1985 Plenum Press, New York

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Nicolson, G.L. (1985). The Evolution of Phenotypic Diversity in Metastatic Tumor Cells. In: Mihich, E. (eds) Biological Responses in Cancer. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1236-9_4

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  • DOI: https://doi.org/10.1007/978-1-4684-1236-9_4

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