Abstract
The Ron-receptor tyrosine kinase has been increasingly recognized for its tumorigenic potential in the last decade. Ron-receptor activation leads to the activation of common receptor tyrosine kinase downstream-signaling pathways, and most prominently in tumor models, activation of MAPK, PI3K and beta-catenin. Numerous experimental models of mammalian tumorigenesis have demonstrated that increased Ron-receptor activity correlates with increased tumorigenesis in a variety of organs of epithelial origin. The evidence for Ron as an oncogene in human tumor biology is growing. The Ron receptor is overexpressed and over activated in a large number of human tumors, and overexpression of Ron correlates with a worse clinical outcome for patients in at least two human cancer states, namely breast and bladder cancer. Several experimental approaches have been demonstrated to successfully block Ron activity and function, and given these convincing data, approaches to block Ron-receptor activity in targeted human cancers should prove to be fruitful in the setting of future clinical research trials.