title: The hedgehog pathway in triple-negative breast cancer.
abstract: Treatment of triple-negative breast cancer (TNBC) remains challenging due to the underlying heterogeneity of this disease coupled with the lack of predictive biomarkers and effective targeted therapies. Intratumoral heterogeneity, particularly enrichment for breast cancer stem cell-like subpopulations, has emerged as a leading hypothesis for systemic therapy resistance and clinically aggressive course of poor prognosis TNBC. A growing body of literature supports the role of the stem cell renewal Hedgehog (Hh) pathway in breast cancer. Emerging preclinical data also implicate Hh signaling in TNBC pathogenesis. Herein, we review the evidence for a pathophysiologic role of Hh signaling in TNBC and explore mechanisms of crosstalk between the Hh pathway and other key signaling networks as well as their potential implications for Hh-targeted interventions in TNBC.
authors.affiliation: Baylor Charles A. Sammons Cancer Center, Dallas, Texas.
authors.forename: Joyce G
authors.initials: JG
authors.lastname: Habib
authors.affiliation: Baylor Charles A. Sammons Cancer Center, Dallas, Texas. joyce.oshaughnessy@usoncology.com.|Texas Oncology, Dallas, Texas. joyce.oshaughnessy@usoncology.com.
authors.forename: Joyce A
authors.initials: JA
authors.lastname: O'Shaughnessy
mesh_terms: D045744:Cell Line, Tumor; D058750:Epithelial-Mesenchymal Transition; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D053823:Hedgehog Proteins / Q000378:metabolism*; D006801:Humans; D014411:Neoplastic Stem Cells / Q000378:metabolism; D015398:Signal Transduction; D064726:Triple Negative Breast Neoplasms / Q000378:metabolism*
chemical_list: D053823:Hedgehog Proteins
keywords: 
  EMT
  ; 
  RTK
  ; 
  TNBC
  ; Breast cancer stem cells; TGF-β; hedgehog; invasion; metastasis