Abstract
FGF receptor (FGFR) signaling is a vital component of both embryonic and postnatal mammary gland development, which has prompted researchers to investigate both its relevance to breast cancer and its potential as a therapeutic target. Deregulated FGFR signaling during breast cancer occurs through various mechanisms, including amplification of the receptor genes, aberrant ligand expression, receptor mutations and translocations. Recent experimental outcomes involving both animal models and human breast cancer cell lines have led to the initiation of multiple early clinical trials investigating the safety and efficacy of small-molecule FGFR inhibitors. In this article, the authors review both the most recent discoveries and the need for further investigation of the mechanisms through which FGF/FGFR signaling has emerged as an oncogenic driver.
Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.