Figure 3.

FGFR dysregulations. There are several mechanisms of oncogenic FGFR function. (A) Gene amplification results in accumulation of FGFRs that usually translate into protein overexpression and activation of the FGFR axis. (B) Gain of function mutations can lead to constitutive FGFR activation with or without FGF binding. (C) Corrupted autocrine and paracrine loops, either via alternative splicing affecting ligand binding specificity or FGFRs getting overstimulated by FGFs produced in an autocrine fashion, by the cancer cells themselves, or by the tumour microenvironment, in a paracrine fashion. (D) Chromosomal rearrangements can lead to the creation of hybrid oncogenic FGFRs by fusing with binding partners at the carboxyl or amino termini. Created with BioRender.com (accessed on 7 November 2021).