The Fibroblast Growth Factor Receptor 1 (FGFR1) is a member of the receptor tyrosine kinase (RTK) family, which plays a crucial role in various cellular processes, including proliferation, differentiation, and survival. FGFR1 is involved in the signaling pathways that regulate embryonic development, tissue repair, and angiogenesis .
The term “FGFR1 Oncogene Partner” refers to the various genes that can fuse with FGFR1 due to chromosomal translocations. These fusion events lead to the creation of chimeric proteins that possess oncogenic properties. One well-known example is the FGFR1-TACC1 fusion, which has been identified in glioblastoma and squamous cell carcinoma (SqCC) .
The fusion proteins resulting from FGFR1 translocations often lead to the constitutive activation of FGFR1 signaling pathways. This activation occurs independently of ligand binding and results in uncontrolled cellular proliferation and inhibition of apoptosis . The FGFR1-TACC1 fusion, for instance, promotes hyperactivation of FGFR1, contributing to tumorigenesis .
Targeting FGFR1 and its fusion proteins has become a promising approach in cancer therapy. Several FGFR inhibitors have been developed and are currently undergoing clinical trials. These inhibitors aim to block the aberrant signaling pathways activated by FGFR1 fusions, thereby inhibiting tumor growth and progression .