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Comment
. 2010 Jan;176(1):25-8.
doi: 10.2353/ajpath.2010.090775. Epub 2009 Nov 30.

Endometrial cells get side-tracked: side population cells promote epithelial-mesenchymal transition in endometrial carcinoma

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Comment

Endometrial cells get side-tracked: side population cells promote epithelial-mesenchymal transition in endometrial carcinoma

Martin Götte. Am J Pathol. 2010 Jan.

Abstract

This Commentary reports on the role of endometrial carcinoma side population cells in epithelial-mesenchymal transition.

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Figures

Figure 1
Figure 1
Contribution of SP cells to endometrial carcinoma pathogenesis. A: EMT, promoted by the high developmental plasticity of stem cells (SC), results in formation of an extracellular matrix (ECM)-rich tumor stroma. B: The tumor stroma serves as a stem cell niche, which is required to maintain the undifferentiated character of the cancer stem cells. C: Through EMT, SP cells loose contact inhibition and acquire a highly migratory phenotype, which facilitates metastasis. D: EMT may promote differentiation to mesenchymal endothelial or mural cells, promoting tumor angiogenesis. E: Angiogenesis will facilitate tumor cell dissemination into the blood stream, thus promoting metastasis. F: Angiogenesis is a prerequisite for primary tumor growth. G: The highly proliferative nature and the unlimited potential for cell division of SP cells displaying a transient amplifying cell phenotype promotes tumor growth. H: The expression of multidrug resistance proteins increases SP cell resistance to chemotherapy (CT).

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