Breast Cancer Res. 2009;11(3):103. Epub 2009 May 20.

Links between transforming growth factor-beta and canonical Wnt signaling yield new insights into breast cancer susceptibility, suppression and tumor heterogeneity.

Incassati A, Pinderhughes A, Eelkema R, Cowin P.

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Department of Cell Biology, New York University School of Medicine, NY, USA. incasa01@nyumc.org

Abstract

In a recent issue of Breast Cancer Research, investigators from the Serra laboratory describe a novel mechanism of transforming growth factor (TGF)-beta tumor suppression. Previously, the authors discovered that stromal TGF-beta signaled through Wnt5a to restrain pubertal ductal elongation and branching. Here, they show that inhibition of stromal TGF-beta signaling or Wnt5a loss leads to increased beta-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.

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Breast Cancer Res. 2009;11(2):R19.

PMID:: 19519951; [PubMed - indexed for MEDLINE]
PMCID: PMC2716492

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