autocrine wnt signaling contributes to breast cancer cell proliferation via the canonical wnt pathway and egfr transactivation自分泌wnt信号有助于乳腺癌细胞增殖通过规范化wnt通路和egfr transactivation.pdfVIP

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autocrine wnt signaling contributes to breast cancer cell proliferation via the canonical wnt pathway and egfr transactivation自分泌wnt信号有助于乳腺癌细胞增殖通过规范化wnt通路和egfr transactivation.pdf

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autocrine wnt signaling contributes to breast cancer cell proliferation via the canonical wnt pathway and egfr transactivation自分泌wnt信号有助于乳腺癌细胞增殖通过规范化wnt通路和egfr transactivation

Available online /content/9/5/R63 Vol 9 No 5 Open Access Research article Autocrine WNT signaling contributes to breast cancer cell proliferation via the canonical WNT pathway and EGFR transactivation 1 1 1 1,2 Thomas Schlange , Yutaka Matsuda , Susanne Lienhard , Alexandre Huber and Nancy E Hynes1 1Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland 2Université de Genève, Département de biologie moléculaire, Sciences II, 30 quai Ernest-Ansermet, CH-1211 Genève 4, Switzerland Corresponding author: Nancy E Hynes, nancy.hynes@fmi.ch Received: 20 Jun 2007 Revisions requested: 3 Aug 2007 Revisions received: 19 Sep 2007 Accepted: 26 Sep 2007 Published: 26 Sep 2007 Breast Cancer Research 2007, 9:R63 (doi:10.1186/bcr1769) This article is online at: /content/9/5/R63 © 2007 Schlange et al ; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background De-regulation of the wingless and integration site breast cancer cell lines with conditioned media, purified growth factor (WNT) signaling pathway via mutations in APC proteins, small-molecule inhibitors, or blocking antibodies. and Axin, proteins that target β-catenin for destruction, have been linked to various types of human cancer. These genetic alterations rarely,