Receptor tyrosine kinases and their activation in melanoma
Easty, David J., Gray, Stephen G., O'Byrne, Kenneth J., O'Donnell, Dearbhaile, & Bennett, Dorothy C. (2011) Receptor tyrosine kinases and their activation in melanoma. Pigment Cell and Melanoma Research, 24(3), pp. 446-461.
Receptor tyrosine kinases (RTKs) and their downstream signalling pathways have long been hypothesized to play key roles in melanoma development. A decade ago, evidence was derived largely from animal models, RTK expression studies and detection of activated RAS isoforms in a small fraction of melanomas. Predictions that overexpression of specific RTKs implied increased kinase activity and that some RTKs would show activating mutations in melanoma were largely untested. However, technological advances including rapid gene sequencing, siRNA methods and phospho-RTK arrays now give a more complete picture. Mutated forms of RTK genes including KIT, ERBB4, the EPH and FGFR families and others are known in melanoma. Additional over- or underexpressed RTKs and also protein tyrosine phosphatases (PTPs) have been reported, and activities measured. Complex interactions between RTKs and PTPs are implicated in the abnormal signalling driving aberrant growth and survival in malignant melanocytes, and indeed in normal melanocytic signalling including the response to ultraviolet radiation. Kinases are considered druggable targets, so characterization of global RTK activity in melanoma should assist the rational development of tyrosine kinase inhibitors for clinical use. © 2011 John Wiley & Sons A/S.
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|Item Type:||Journal Article|
|Keywords:||Melanoma, Phospho-array, Signal transduction, Target, Tyrosine kinase, Tyrosine phosphatase, ephrin receptor A2, epidermal growth factor receptor 4, erlotinib, fibroblast growth factor receptor, gefitinib, imatinib, phosphatidylinositol 3 kinase, phospholipase C gamma, protein tyrosine kinase, protein tyrosine kinase inhibitor, protein tyrosine phosphatase, protein tyrosine phosphatase 2b, Ras protein, small interfering RNA, somatomedin C receptor, unclassified drug, cancer growth, cell survival, chronic myeloid leukemia, enzyme activation, gene mutation, gene overexpression, gene sequence, genetic variability, human, melanocyte, nonhuman, protein expression, protein interaction, review, ultraviolet radiation, Animals, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Humans, Melanocytes, Mutation, Neoplasm Proteins, Protein Tyrosine Phosphatases, Receptor Protein-Tyrosine Kinases, Animalia|
|Divisions:||Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
|Copyright Owner:||Copyright 2011 Wiley-Blackwell Publishing, Inc.|
|Deposited On:||02 Dec 2013 06:20|
|Last Modified:||13 Mar 2014 05:13|
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