While it is very clear that activation of β-catenin through the canonical Wnt-pathway plays a role in a multitude of human cancers, it has also been noted time and time again that activation of β-catenin is observed in tumors without any clear mutation in any of the major components of the pathway or any increase in Wnt signaling. This suggests that other factors maybe capable of inducing activation and downstream signaling via β-catenin. Indeed, multiple growth factor and developmental signaling pathways have been found to transactivate β-catenin. It is also reasonable to consider the converse: that the Wnt pathway is capable of transactivating other signaling pathways. In fact, multiple studies have outlined the capability of Wnt signaling to activate other pathways in various types of cancer. Such association has led to the initiative to develop approaches to therapy that are capable of targeting both the Wnt pathway and the pathways it crosstalks with simultaneously. The crosstalk that occurs between Wnt and other signaling pathways will be explored in this chapter with a primary focus on how these pathways interact in the development and progression of cancer.

Original languageEnglish
Title of host publicationTargeting the Wnt Pathway in Cancer
PublisherSpringer New York
Number of pages30
ISBN (Print)9781441980229
StatePublished - Dec 1 2011


  • Cancer
  • Cox-2
  • Crosstalk
  • Development
  • Growth
  • Growth factor
  • Hedgehog
  • Metastasis
  • Notch
  • PI3K
  • Proliferation
  • Ras
  • Receptor tyrosine
  • Signaling
  • Suppression
  • Transactivation
  • Wnt
  • kinase
  • mTOR


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