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. 2014 Oct 11;12:271. doi: 10.1186/s12967-014-0271-5

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© Touboul et al.; licensee BioMed Central Ltd. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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The cytokine-mediated crosstalk between Mesenchymal Stem Cells (MSCs) and Ovarian Cancer Cells (OCCs) leads to a shift in MSCs phenotype resulting in tumorigenesis promotion. MSCs are recruited to tumor stroma from a peri-vascular niche. Their engraftment is associated with phenotypic modulations in response to tumor-derived secreted factors. Primed MSCs support tumor growth and self-renewal. Their differentiation in cancer-associated fibroblasts (CAFs) contributes to stromal modifications suitable for tumor expansion and stimulates angiogenesis. We highlight the role of HOXA9 expression that results in transcriptional activation of the gene encoding TGFβ2 inducing in turn CAFs expression VEGF.