Overexpression and functional alterations of the EphA2 tyrosine kinase in cancer.
Cancer is a disease of aberrant signal transduction. The expression and function of intracellular signaling pathways are frequently subverted as cells progress towards a metastatic phenotype. In particular, tyrosine kinases initiate powerful signals that govern many different aspects of cell behavior. In Recent studies have demonstrated that the EphA2 receptor tyrosine kinase is frequently overexpressed and functionally altered in aggressive tumor cells, and that these changes promote metastatic character. Herein, we provide an overview of our current understanding of EphA2, with emphasis upon the differential regulation of EphA2 expression and function. We also show that differential EphA2 expression and function may provide a unique opportunity for selective therapeutic targeting of EphA2 in metastatic disease.
Kinch
Michael S
MS
MedImmune, Inc., Gaithersburg, Maryland 20878, USA. kinchm@medimmune.com
Carles-Kinch
Kelly
K
D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008954:Models, Biological; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009420:Nervous System / Q000196:embryology / Q000201:enzymology / Q000254:growth & development; D036104:Receptor, EphA2 / Q000235:genetics / Q000378:metabolism* / Q000502:physiology
D036104:Receptor, EphA2