title: Functional Crosstalk Between WNT Signaling and Tyrosine Kinase Signaling in Cancer.
abstract: Extensive molecular characterization of tumors has revealed that the activity of multiple signaling pathways is often simultaneously dampened or enhanced in cancer cells. Aberrant WNT signaling and tyrosine kinase signaling are two pathways that are frequently up- or downregulated in cancer. Although signaling pathways regulated by WNTs, tyrosine kinases, and other factors are often conceptualized as independent entities, the biological reality is likely much more complex. Understanding the mechanisms of crosstalk between multiple signal transduction networks is a key challenge for cancer researchers. The overall goals of this review are to describe mechanisms of crosstalk between WNT and tyrosine kinase pathways in cancer and to discuss how understanding intersections between WNT and tyrosine kinase signaling networks might be exploited to improve current therapies.
authors.affiliation: Harvard Medical School Department of Cell Biology, Boston, MA; Boston Children's Hospital Division of Newborn Medicine, Boston, MA. Electronic address: jamie.anastas@childrens.harvard.edu.
authors.forename: Jaimie N
authors.initials: JN
authors.lastname: Anastas
mesh_terms: D006801:Humans; D058990:Molecular Targeted Therapy / Q000379:methods; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D011505:Protein-Tyrosine Kinases / Q000378:metabolism*; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism; D057050:Receptor Tyrosine Kinase-like Orphan Receptors / Q000378:metabolism; D015398:Signal Transduction; D060449:Wnt Signaling Pathway; D051176:beta Catenin / Q000378:metabolism
chemical_list: C495270:CTNNB1 protein, human; D051176:beta Catenin; D011505:Protein-Tyrosine Kinases; C080836:RYK protein, human; D020794:Receptor Protein-Tyrosine Kinases; D057050:Receptor Tyrosine Kinase-like Orphan Receptors