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Links between transforming growth factor-β and canonical Wnt signaling yield new insights into breast cancer susceptibility, suppression and tumor heterogeneity
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....
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2716492/ https://www.ncbi.nlm.nih.gov/pubmed/19519951 http://dx.doi.org/10.1186/bcr2253 |
Sumario: | 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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