Links between transforming growth factor-β and canonical Wnt signaling yield new insights into breast cancer susceptibility, suppression and tumor heterogeneity
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* Corresponding author: Pamela Cowin cowinp01@nyumc.org
1 Department of Cell Biology, New York University School of Medicine, New York, USA
2 Department of Dermatology, New York University School of Medicine, New York, USA
3 Department of Pathology, New York University School of Medicine, New York, USA
Breast Cancer Research 2009, 11:103 doi:10.1186/bcr2253
Published: 20 May 2009Abstract
In a recent issue of Breast Cancer Research, investigators from the Serra laboratory describe a novel mechanism of transforming growth factor (TGF)-β tumor suppression. Previously, the authors discovered that stromal TGF-β signaled through Wnt5a to restrain pubertal ductal elongation and branching. Here, they show that inhibition of stromal TGF-β signaling or Wnt5a loss leads to increased β-catenin transcriptional activity and reduced latency in mammary tumor models, with tumors displaying a higher proportion of progenitor cell markers. These findings reveal a novel intersection of two tumor suppressors with a potent oncogenic pathway and highlight the need for further study on the role played by canonical Wnt signaling in breast cancer susceptibility and subtype.