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lüll 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 PBreast Cancer Res 2009[]; 11 (3): 103In 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.|*Gene Expression Regulation, Neoplastic[MESH]|*Genetic Predisposition to Disease[MESH]|Animals[MESH]|Breast Neoplasms/*metabolism[MESH]|Female[MESH]|Humans[MESH]|Medical Oncology[MESH]|Proto-Oncogene Proteins/metabolism[MESH]|Signal Transduction[MESH]|Transforming Growth Factor beta/*metabolism[MESH]|Wnt Proteins/*metabolism[MESH]|Wnt-5a Protein[MESH] |