Why targeted therapy hasn't worked in advanced cancer

• Type of Material: Article
• Authors: Jack Arbiser, Emory University
• Language: English
• Date: 2007-10-01
• Publisher: American Society for Clinical Investigation
• Publication Version: Final Published Version
• Copyright Statement: © 2007, American Society for Clinical Investigation
• Final Published Version (URL): http://www.jci.org/articles/view/33190
• Title of Journal or Parent Work: Journal of Clinical Investigation
• ISSN: 0021-9738
• Volume: 117
• Issue: 10
• Start Page: 2762
• End Page: 2765
• Research Categories: Health Sciences, Rehabilitation and Therapy; Health Sciences, Oncology; Health Sciences, General

Abstract

In this issue of the JCI, Nissen et al. report that a reciprocal interaction exists between the growth factors FGF2 and PDGF-BB, causing tumors to exhibit increased angiogenesis and metastatic potential (see the related article beginning on page 2766). Both FGF2 and PDGF-BB signal through tyrosine kinase receptors, which have been the target of tyrosine kinase inhibitors for cancer therapies. These inhibitors are usually small molecules that inhibit the kinase activity of a receptor or nonreceptor tyrosine kinase, preventing downstream signaling. The results of this study shed light on why tyrosine kinase inhibitors have been useful for the treatment of only a small number of advanced cancers. Currently, a major focus of pharmaceutical companies is to develop ever more potent and specific tyrosine kinases. The results presented here suggest that this approach may not be successful.