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editorial

. 2015 Mar 19;14(6):793–794. doi: 10.1080/15384101.2015.1010968

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

© Mieke Van Bockstal, Louis Libbrecht, and Olivier De Wever

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — Ductal carcinoma in situ (DCIS) causes growth factor-induced transition of fibroblasts into cancer-associated fibroblasts (CAF). CAF-induced ECM remodeling turns sclerotic stroma into myxoid stroma. Decreased decorin expression and increased versican expression may contribute to this altered architecture. Alpha-smooth muscle actin (α-SMA) is differentially regulated by bFGF and TGF-β1. This CAF-induced altered ECM composition paves the path for invasion.