| Literature DB >> 27992319 |
Abstract
Fibroblast growth factor (FGF) signaling through its receptors, FGFR1, FGFR2, FGFR3, or FGFR4, regulates cell fate, angiogenesis, immunity, and metabolism. Dysregulated FGF signaling causes human diseases, such as breast cancer, chondrodysplasia, gastric cancer, lung cancer, and X-linked hypophosphatemic rickets. Recombinant FGFs are pro-FGF signaling therapeutics for tissue and/or wound repair, whereas FGF analogs and gene therapy are under development for the treatment of cardiovascular disease, diabetes, and osteoarthritis. FGF traps, anti-FGF/FGFR monoclonal antibodies (mAbs), and small-molecule FGFR inhibitors are anti-FGF signaling therapeutics under development for the treatment of cancer, chondrodysplasia, and rickets. Here, I discuss the benefit-risk and cost-effectiveness issues of precision medicine targeting FGFRs, ALK, EGFR, and FLT3. FGFR-targeted therapy should be optimized for cancer treatment, focusing on genomic tests and recurrence.Entities:
Keywords: epithelial-to-mesenchymal transition; erdafitinib; immune-checkpoint blocker; infigratinib; miRNA; myeloproliferative syndrome.
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Year: 2016 PMID： 27992319 DOI： 10.1016/j.tips.2016.10.003
Source DB: PubMed Journal: Trends Pharmacol Sci ISSN： 0165-6147 Impact factor: 14.819