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Epithelial-Mesenchymal Interactions in Cancer (Paperback, Softcover reprint of the original 1st ed. 1995)
Loot Price: R1,487
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Epithelial-Mesenchymal Interactions in Cancer (Paperback, Softcover reprint of the original 1st ed. 1995)
Series: Experientia Supplementum, 74
Expected to ship within 10 - 15 working days
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Total price: R1,507
Discovery Miles: 15 070
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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.
General
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