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01.06.2009 | Editorial | Ausgabe 3/2009

Breast Cancer Research 3/2009

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

Breast Cancer Research > Ausgabe 3/2009
Angela Incassati, Alicia Pinderhughes, Rachel Eelkema, Pamela Cowin
Wichtige Hinweise

Competing interests

The authors declare that they have no competing interests.


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.

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