Fibroblast Growth Factor Receptor Alterations in Glioblastoma
Summary
Fibroblast growth factor receptors (FGFRs) constitute a family of transmembrane tyrosine kinases that regulate cellular proliferation, differentiation and survival. In glioblastoma, alterations of FGFR1, FGFR2 and FGFR3 occur in roughly 8 per cent of cases and include gene amplifications, point mutations and oncogenic fusions. Such aberrations drive tumour heterogeneity, promote invasive behaviour and sustain glioblastoma stem-like populations that resist conventional therapies. FGFR1 overexpression has been linked to enhanced cell migration and radioresistance, whereas FGFR3-TACC3 fusions confer constitutive kinase activity, genomic instability and altered metabolic programmes. These molecular changes delineate distinct biological subgroups of glioblastoma with characteristic histological and epigenetic profiles. Clinically, FGFR alterations offer both prognostic insight and the potential for precision medicine. Small-molecule inhibitors targeting FGFR kinase domains have shown proof-of-concept activity, although efficacy varies with the specific alteration. Stratification of patients by FGFR genotype and integration of multi-omic biomarkers are emerging as crucial steps towards tailored therapeutic strategies in this aggressive brain cancer.
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Fibroblast Growth Factor Receptor Alterations in Glioblastoma publication trend
The graph below shows the total number of articles in fibroblast growth factor receptor alterations in glioblastoma across all publications each year (not limited to Nature Index journals).
Technical terms
Fibroblast Growth Factor Receptor (FGFR): A family of receptor tyrosine kinases that mediate signals for cell growth and survival upon binding fibroblast growth factors.
FGFR3-TACC3 fusion: An oncogenic gene rearrangement that fuses the kinase domain of FGFR3 to the TACC3 protein, resulting in constitutive receptor activation and tumourigenic signalling.
IDH-wildtype: Denotes glioblastomas lacking mutations in isocitrate dehydrogenase genes, typically associated with more aggressive clinical behaviour.
Tyrosine kinase inhibitor: A small-molecule drug that blocks the enzymatic activity of receptor or non-receptor tyrosine kinases, disrupting downstream oncogenic pathways.
References
- Spatial distribution and functional relevance of FGFR1 and FGFR2 expression for glioblastoma tumor invasion. Cancer Letters (2023).
- Clinico-pathological and epigenetic heterogeneity of diffuse gliomas with FGFR3::TACC3 fusion. Acta Neuropathologica Communications (2023).
- Infigratinib in Patients with Recurrent Gliomas and FGFR Alterations: A Multicenter Phase II StudyInfigratinib in recurrent gliomas with FGFR alterations. Clinical Cancer Research (2022).
- Fibroblast Growth Factor Receptor Functions in Glioblastoma. Cells (2019).
- Diffuse Gliomas with FGFR3-TACC3 Fusions: Oncogenic Mechanisms, Hallmarks, and Therapeutic Perspectives. Cancers (2023).
- FGFR1/FOXM1 pathway: a key regulator of glioblastoma stem cells radioresistance and a prognosis biomarker. Oncotarget (2018).
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