title: Is there more to Wnt signalling in breast cancer than stabilisation of beta-catenin?
abstract: Increased Wnt signalling has been implicated in the aetiology of many different human cancers, including breast cancers. In most cases, Wnt signalling is thought to drive tumourigenesis through the stabilisation of cytosolic beta-catenin and the subsequent changes in the expression of T-cell factor (TCF)-dependent genes. However, this is not necessarily the only mechanism, as Wnt proteins can signal through a number of different intracellular signalling pathways. The ongoing work from Nancy Hynes' laboratory continues to highlight this latter possibility.
authors: Giovanna M
authors: GM
authors: Collu
authors: Olivier
authors: O
authors: Meurette
authors: Keith
authors: K
authors: Brennan
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000503:physiopathology*; D045744:Cell Line, Tumor / Q000637:transplantation; D066246:ErbB Receptors / Q000502:physiology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000502:physiology; D005260:Female; D051157:Frizzled Receptors / Q000502:physiology; D006801:Humans; D051379:Mice; D009363:Neoplasm Proteins / Q000502:physiology*; D009368:Neoplasm Transplantation; D015398:Signal Transduction; D051153:Wnt Proteins / Q000502:physiology*; D051176:beta Catenin / Q000502:physiology*
chemical_list: D051157:Frizzled Receptors; D009363:Neoplasm Proteins; D051153:Wnt Proteins; D051176:beta Catenin; C512478:EGFR protein, human; C541485:EGFR protein, mouse; D066246:ErbB Receptors; D048049:Extracellular Signal-Regulated MAP Kinases