The fibroblast growth factor receptor 2 (FGFR2) gene is located at chromosome 10q26 and encodes two major isoforms, FGFR2b and FGFR2c, which act as FGF receptors with different functional domains and ligand specificities. The FGFR2 protein belongs to a superfamily of four membrane-bound receptor tyrosine kinases (RTKs), which includes FGFR1, FGFR2, FGFR3, and FGFR4 and exhibits biological activity by interacting with fibroblast growth factor (FGF) ligands.

FGFR2 is extensively expressed in various tissues and involved in a wide variety of biologic activities and cellular functions, including cell proliferation, differentiation, survival, adhesion, migration, motility and apoptosis, and processes such as bone formation, wound healing, tumorigenesis, angiogenesis, vasculogenesis and blood vessel remodeling. In addition to the basic experiments, clinical data from the cases of congenital skeletal disorders show FGFR2 mutation is related to skin phenotypes, including acne, cutis gyrata, and acanthosis nigricans. Moreover, FGFR2 mutations or variations occur in various kinds of cancers including estrogen receptor-positive breast cancer, diffuse-type gastric cancer, and endometrial uterine cancer. Accordingly, FGFR2 abnormalities result in a spectrum of bone and skin pathologies as well as several types of cancer.

Although FGFR2 signaling has been extensively studied, and preclinical evidence indicates that genetic alterations of FGFR2 are often common in various diseases, there is an urgent need to understand the molecular mechanisms of FGFR2 abnormalities. This knowledge will surely contribute to the identification of potential therapeutic approaches. This special issue aims to explore the molecular mechanisms of FGFR2 abnormalities. We would like to invite all investigators working on FGFR2 using in vitro and in vivo methods in human and animal species to share their knowledge about the potential mechanisms underlying FGFR2 abnormalities in the spectrum of bone-formation, skin pathologies and human cancers.