ArticleActa neuropathologica communications2021
Novel targetable FGFR2 and FGFR3 alterations in glioblastoma associate with aggressive phenotype and distinct gene expression programs.
Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 40 citations in OpenAlex.
- Exploring the landscape of targetable alterations in patients with glioblastoma.Nature reviews. Clinical oncology · 2026Review
- Cancer signaling networks in tumor progression and drug resistance: Crosstalk, adaptive reprogramming and therapeutic targeting (Review).Oncology reports · 2026Review
- FGFR alterations and potential role of FGFR inhibitors in pediatric brain tumors.Neuro-oncology advances · 2026Review
- Integrative Machine-Learning Molecular Subtyping and Risk Scores of Circadian Rhythm-Related Prognostic Signatures in Colorectal Cancer.Journal of gastrointestinal cancer · 2026Article
- Identification of natural FGFR3 inhibitor for glioma using integrated computational and microRNA regulatory analysis.Scientific reports · 2026Article
- Review
- Role of matrix metalloproteinases in the invasion of glioblastoma and drug interventions (Review).International journal of molecular medicine · 2026Review
- MGMT, NUPR1, NDRG2, and GLI1 Gene Promoter Methylation in Glioblastoma Tissues and Association with Clinical Characteristics and Therapeutic Outcomes.International journal of molecular sciences · 2026Article
- Calcifying pseudoneoplasm of the neuraxis progressing to G5/PDGFRA subgroup glioblastoma in a United States Army veteran with a history of head trauma and germline POT1 and EPHB2 mutations: illustrative case.Journal of neurosurgery. Case lessons · 2025Article
- Review
- Metabolism and signaling crosstalk in glioblastoma progression and therapy resistance.Molecular oncology · 2025Review
- Novel Fibroblast Growth Factor Receptor 3-Fatty Acid Synthase Gene Fusion in Recurrent Epithelioid Glioblastoma Linked to Aggressive Clinical Progression.Current oncology (Toronto, Ont.) · 2024Article
- Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024Review
- Clinical features, MRI, molecular alternations, and prognosis of astrocytoma based on WHO 2021 classification of central nervous system tumors: A single-center retrospective study.Cancer medicine · 2024Article
- FGFR-targeted therapeutics: clinical activity, mechanisms of resistance and new directions.Nature reviews. Clinical oncology · 2024Review
- Article
- Adult glioblastoma with Lynch syndrome-associated mismatch repair deficiency forms a distinct high-risk molecular subgroup.Free neuropathology · 2024Article
- From signalling pathways to targeted therapies: unravelling glioblastoma's secrets and harnessing two decades of progress.Signal transduction and targeted therapy · 2023Review
- SPRY4-dependent ERK negative feedback demarcates functional adult stem cells in the male mouse germline†.Biology of reproduction · 2023Article
- Leptomeningeal neuraxis relapse in glioblastoma is an uncommon but not rare event associated with poor outcome.BMC neurology · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prognostic molecular subgrouping of glioblastoma is an ongoing effort and the current classification includes IDH-wild-type and IDH-mutant entities, the latter showing significantly better prognosis. We performed a comparative integrated analysis of the FGFR glioblastoma subgroup consisting of 5 cases from a prospective 101-patient-cohort. FGFR alterations included FGFR2-TACC2 and FGFR2 amplifications arising in a multifocal IDH-mutant glioblastoma with unexpected 2.5-month patient survival, novel FGFR3 carboxy-terminal duplication and FGFR3-TLN1 fusion, and two previously described FGFR3-TACC3 fusions. The FGFR2 tumors showed additional mutations in SERPINE1/PAI-1 and MMP16, as part of extensive extracellular matrix remodeling programs. Whole transcriptomic analysis revealed common proliferation but distinct morphogenetic gene expression programs that correlated with tumor histology. The kinase program revealed EPHA3, LTK and ALK receptor tyrosine kinase overexpression in individual FGFR tumors. Paradoxically, all FGFR-fused glioblastomas shared strong PI3K and MAPK pathway suppression effected by SPRY, DUSP and AKAP12 inhibitors, whereas the FGFR2-TACC2 tumor elicited also EGFR suppression by ERRFI1 upregulation. This integrated analysis outlined the proliferation and morphogenetic expression programs in FGFR glioblastoma, and identified four novel, clinically targetable FGFR2 and FGFR3 alterations that confer aggressive phenotype and trigger canonical pathway feedback inhibition, with important therapeutic implications.
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