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Synopsis
The contribution of epithelia-mesenchyme interaction to normal development (eg., tissue formation) and to neoplasia has become a subject of increasing interest to scientists because of recent progress in deciphering the molecular signals that mediate this interaction. Clearly, some of the same types of molecules (eg., growth factors and their receptors, proteolytic enzymes, cell adhesion molecules, and structural proteins of the extracellular matrix) mediate exchange of information between epithelia and mesenchyme during normal development and malignant growth. However, defects in the regulation of this exchange appear to contribute to malignancy by allowing growth promoting, invasogenic, and angiogenic factors to accumulate within the microenvironment of the tumor. For example, recent studies suggest that abnormal interactions between tumor epithelial cells and stromal mesenchymal cells contribute to the overproduction and accumulation of scatter factor (hepatocyte growth factor), an invasogenic and angiogenic cytokine, in certain types of tumor. The production and and activation of type IV collagenase, a matrix-degrading enzyme required for tumor cell invasion, appears to require intimate cooperation between tumor and stromal cells. The material contained in this volume highlights the state-of-the-art of knowledge of the molecular mechanisms by which epithelia and mesenchyme collaborate, and the abnormalities in these mechanisms that may lead to the development of cancer.
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Epithelial?Mesenchymal Interactions in Cancer (Experientia Supplementum)
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Epithelial?Mesenchymal Interactions in Cancer
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EpithelialMesenchymal Interactions in Cancer (Paperback)
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Paperback. Condition: new. Paperback. gar discusses recent studies of the SF gene promoter that may be relevant to understanding the detailed molecular mechanism(s) by which soluble factors regulate SF production. Polverini and Nickoloff discuss another mechanism by which SF may enhance tumor growth, ie., stimulation of angiogenesis, the formation of new blood vessels from pre-existing microvessels. Angiogenesis is required for continued growth of most solid tumors, and provides a mechanism by which the stroma may continue to grow along with the tumor cells. Although endothelial cells are stromal cells, they express a number of epithelial characteristics including (i) epithelial-like tight junctions and junctional proteins; (ii) the ability to organize into flat- tened tubular structures; (iii) the c-met receptor protein; and (iv) biologic responsiveness to SF. It is, perhaps, not surprising that vascular endothe- lial cells may both produce and respond to SF in different situations. 'Epithelialness' may be defined in two ways: (i) expression of generic epithelial structures and proteins (eg., specialized junctions, junctional proteins [eg., cadherins, ZOl], cytokeratins); and (ii) production of specific differentiated products (eg., milk proteins by mammary epithelia, renin by renal tubular epithelia of the juxtaglomerular apparatus). Recent studies suggest that SF Ic-met signalling may mediate epithelia- mesenchyme interconversion, in part by modifying some of the generic epithelial characteristics. Nusrat discusses the effects of SF on the epithelial junctional apparatus. Relatively little is known about whether and how SF regulates cell-specific differentiation. The contribution of epithelia-mesenchyme interaction to normal development (eg., tissue formation) and to neoplasia has become a subject of increasing interest to scientists because of recent progress in deciphering the molecular signals that mediate this interaction. Clearly, some of the same types of molecules (eg., growth factors and their receptors, proteolytic enzymes, cell adhesion molecules, and structural proteins of the extracellular matrix) mediate exchange of information between epithelia and mesenchyme during normal development and malignant growth. However, defects in the regulation of this exchange appear to contribute to malignancy by allowing growth promoting, invasogenic, and angiogenic factors to accumulate within the microenvironment of the tumor. For example, recent studies suggest that abnormal interactions between tumor epithelial cells and stromal mesenchymal cells contribute to the overproduction and accumulation of scatter factor (hepatocyte growth factor), an invasogenic and angiogenic cytokine, in certain types of tumor. The production and and activation of type IV collagenase, a matrix-degrading enzyme required for tumor cell invasion, appears to require intimate cooperation between tumor and stromal cells. The material contained in this volume highlights the state-of-the-art of knowledge of the molecular mechanisms by which epithelia and mesenchyme collaborate, and the abnormalities in these mechanisms that may lead to the development of cancer. Shipping may be from multiple locations in the US or from the UK, depending on stock availability. Seller Inventory # 9783034898935
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Epithelial?Mesenchymal Interactions in Cancer
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Epithelial?Mesenchymal Interactions in Cancer (Experientia Supplementum)
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Epithelial?Mesenchymal Interactions in Cancer
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Epithelial-Mesenchymal Interactions in Cancer
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Birkhäuser Basel, Birkhäuser Sep 2011, 2011
ISBN 10: 3034898932
ISBN 13: 9783034898935
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Taschenbuch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -gar discusses recent studies of the SF gene promoter that may be relevant to understanding the detailed molecular mechanism(s) by which soluble factors regulate SF production. Polverini and Nickoloff discuss another mechanism by which SF may enhance tumor growth, ie., stimulation of angiogenesis, the formation of new blood vessels from pre-existing microvessels. Angiogenesis is required for continued growth of most solid tumors, and provides a mechanism by which the stroma may continue to grow along with the tumor cells. Although endothelial cells are stromal cells, they express a number of epithelial characteristics including (i) epithelial-like tight junctions and junctional proteins; (ii) the ability to organize into flat tened tubular structures; (iii) the c-met receptor protein; and (iv) biologic responsiveness to SF. It is, perhaps, not surprising that vascular endothe lial cells may both produce and respond to SF in different situations. 'Epithelialness' may be defined in two ways: (i) expression of generic epithelial structures and proteins (eg., specialized junctions, junctional proteins [eg., cadherins, ZOl], cytokeratins); and (ii) production of specific differentiated products (eg., milk proteins by mammary epithelia, renin by renal tubular epithelia of the juxtaglomerular apparatus). Recent studies suggest that SF Ic-met signalling may mediate epithelia mesenchyme interconversion, in part by modifying some of the generic epithelial characteristics. Nusrat discusses the effects of SF on the epithelial junctional apparatus. Relatively little is known about whether and how SF regulates cell-specific differentiation. 316 pp. Englisch. Seller Inventory # 9783034898935
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Epithelial?Mesenchymal Interactions in Cancer
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Epithelial?Mesenchymal Interactions in Cancer
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Epithelial-Mesenchymal Interactions in Cancer
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Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Epithelial-mesenchymal transitions in development and tumor progression.- Regulation of scatter factor (hepatocyte growth factor) production by tumor-stroma interaction.- Regulation of HGF and HGFR gene expression.- The role of scatter factor and the c-met . Seller Inventory # 4319695
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