Abstract
The acquisition of the ability to metastasize is the ultimate and most deadly level of the tumorigenic progression. Metastatic cells are able to dissociate from the primary tumor, invade through the surrounding tissue and endothelial layer into the bloodstream, migrate through the bloodstream to the site of metastasis and then reinvade and proliferate to generate a new tumor lesion (Poste and Fidler 1980). Throughout this process the metastatic cell assumes a number of different morphological configurations varying from densely packed within the tumor mass, deformed and elongated in invasion, and free-floating in the bloodstream. During each of these stages it must acquire distinct functional capabilities requiring the expression of distinct molecular entities.
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References
Altevogt P, Fogel M, Cheiengsong-Popov R, Dennis J, Robinson P, Schirrmacher V (1983) Different patterns of lectin binding and cell surface sialylation detected on related high-and low-metastatic tumor lines. Cancer Res 43:5138–5144
Ben-Ze’ev A, Farmer SR, Penman S (1980) Protein synthesis requires cell-surface contact while nuclear events respond to cell shape in anchorage dependant fibroblasts. Cell 21:365–372
Brouty-Boye D, Tucker RW, Folkman J (1980) Transformed and neoplastic phenotype reversibility during culture by cell density and cell shape. Int J Cancer 26:501–507
Fogel M, Altevogt P, Schirrmacher V (1983) Metastatic potential severely altered by changes in tumor cell adhesiveness and cell surface sialylation. J Exp Med 157:371–376
Folkman J, Greenspan HP (1975) Influence of geometry on control of cell growth. Biochim Biophys Acta 417:211–236
Folkman J, Moscona A (1978) Role of cell shape in growth control. Nature 273:345–349
Hochman Y, Katz A, Levy E, Eshel S (1981) Substrate adhering lymphoid cells show impaired tumorigenicity and increased immunogenicity. Nature 290:248–249
Laferte S, Dennis JW (1988) Glycosylation-dependant collagen-binding activities of two membrane glycoproteins in MDAY-D2 tumor cells. Cancer Res 48:4743–4748
Maroudas NG (1973) Growth of fibroblasts on linear and planar anchorage of limiting dimensions. Exp Cell Res 81:104–110
Matzku S, Komitowski D, Mildenberger M, Zoller M (1983) Characterization of BSp73, a spontaneous rat tumor and its in vivo selected variants showing different metastasizing capacities. Invasion Metastasis 3:109–123
Nabi IR, Raz A (1987) Cell shape modulation alters glycosylation of a metastatic melanoma cell surface antigen. Int J Cancer 40:396–402
Nabi IR, Raz A (1988) Loss of metastatic responsiveness to cell shape modulation in a newly characterized B16 melanoma adhesive variant. Cancer Res 48:1258–1264
Nicolson GL (1982) Cancer metastasis. Organ colonization and the cell surface properties of malignant cells. Biochim Biophys Acta 695:113–176
Poste G, Fidler IJ (1980) The pathogenesis of cancer metastasis. Nature 283:139–146
Raz A, Ben-Ze’ev A (1982) Growth control and cell spreading: differential response in preneoplastic and in metastatic variants. Int J Cancer 29:711–715
Raz A, Ben-Ze’ev A (1983) Modulation of the metastatic capability in B16 melanoma by cell shape. Science 221:1307–1310
Schirrmacher V, Altevogt P, Fogel M, Dennis J, Waller CA, Barz D, Schwartz R, et a. (1982) Importance of cell surface carbohydrates in cancer cell adhesion, invasion, and metastasis. Invasion Metastasis 2:313–360
Shiu RP, Paterson JA (1984) Alteration of cell shape, sadhesion, and lipid accumulation in human breast cancer cells (T-4D7) by human prolactin and growth hormone. Cancer Res 44:1178–1186
Smets LA, van Beek WP (1984) Carbohydrate of the tumor cell surface. Biochim Biophys Acta 738:237–249
Stackpole CW, Fornbaio DM, Alterman AL (1985) Phenotypic interconversion of B16 melanoma clonal cell population: Relationship between metastasis and tumor growth rate. Int J Cancer 35:667–674
Stoker M, O’Neill CH, Berryman S, Waxman V (1968) Anchorage and growth regulation in normal and virus-transformed cells. Int J Cancer 3:683–693
Takenaga K (1984) Enhanced metastatic potential of cloned low metastatic Lewis lung carcinoma cells treated in vitro with dimethyl sulfoxide. Cancer Res 44:1122–1127
Warren L, Buck CA, Tusynski GP (1978) Glycopeptide changes and malignant transformation: a possible role for carbohydrate in malignant behavior. Biochim Biophys Acta 738:237–249
Wittelsberger SC, Kleene K, Penman S (1981) Progressive loss of shape responsive metabolic controls in cells with increasingly transformed phenotype. Cell 24:859–866
Young RM, Newby M, Meunier J (1985) Relationship between morphology, dissemination, migration and prostaglandin E2 secretion by cloned variants of Lewis lung carcinoma. Cancer Res 45:3918–3923
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© 1989 Springer-Verlag Berlin Heidelberg
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Nabi, I.R., Raz, A. (1989). Cell Shape and the Metastatic Phenotype. In: Schirrmacher, V., Schwartz-Albiez, R. (eds) Cancer Metastasis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74236-1_12
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DOI: https://doi.org/10.1007/978-3-642-74236-1_12
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-50471-9
Online ISBN: 978-3-642-74236-1
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