ArticleCancer cell international2022
FGFR1 is a potential therapeutic target in neuroblastoma.
Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- CircGABRB2_006 Drives Malignant Progression and EMT in Papillary Thyroid Carcinoma via the miR-296-5p/FGFR1 Axis.Biochemical genetics · 2026Article
- Mutated FGFR1 is an oncogenic driver and therapeutic target in high-risk neuroblastoma.The Journal of clinical investigation · 2026Article
- Sprouty in Tumors of the Nervous System.International journal of molecular sciences · 2025Review
- Advances in Targeting Growth Factor Signalling in Neuroblastoma and Overcoming Drug Resistance.Cells · 2025Review
- Concurrence of FGFR1 mutations modulates oncogenesis in glioneuronal tumors.The EMBO journal · 2025Article
- Chromosomal instability degrades developmental phenotypes essential for anti-GD2 immunotherapy outcomes in high-risk neuroblastoma.Cell reports. Medicine · 2025Article
- The Non-Coding Regulatory Variant rs2863002 at chr11p11.2 Increases Neuroblastoma Risk by Affecting HSD17B12 Expression and Lipid Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Potential Cause-and-Effect Relationship between Gut Microbiota and Childhood Neuroblastoma: A Mendelian Randomization Analysis.Indian journal of pediatrics · 2025Article
- Selective degradation of FGFR1/2 overcomes antiestrogen resistance in ER+ breast cancer with FGFR1/2 alterations.Cancer letters · 2025Article
- Regulatory non-coding somatic mutations as drivers of neuroblastoma.British journal of cancer · 2025Article
- Pharmacological and Biological Targeting of FGFR1 in Cancer.Current issues in molecular biology · 2024Review
- Integrative genomic analyses identify neuroblastoma risk genes involved in neuronal differentiation.Human genetics · 2024Article
- A High-Grade Glioma, Not Elsewhere Classified in an Older Adult with Discordant Genetic and Epigenetic Analyses.Biomedicines · 2024Article
- Targeting FGFR for cancer therapy.Journal of hematology & oncology · 2024Review
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Genomic Analysis Made It Possible to Identify Gene-Driver Alterations Covering the Time Window between Diagnosis of Neuroblastoma 4S and the Progression to Stage 4.International journal of molecular sciences · 2022Article
- Pro-metastatic and mesenchymal gene expression signatures characterize circulating tumor cells of neuroblastoma patients with bone marrow metastases and relapse.Frontiers in oncology · 2022Article
- Fibroblast growth factor receptor 1 gene mutation as a potential risk factor for spontaneous intracranial hemorrhage in pediatric low-grade glioma patients.Neuro-oncology advancesArticle
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Authors and funding
14 authors at 6 institutions in 1 country.
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Abstract
backgroundFGFR1 regulates cell-cell adhesion and extracellular matrix architecture and acts as oncogene in several cancers. Potential cancer driver mutations of FGFR1 occur in neuroblastoma (NB), a neural crest-derived pediatric tumor arising in sympathetic nervous system, but so far they have not been studied experimentally. We investigated the driver-oncogene role of FGFR1 and the implication of N546K mutation in therapy-resistance in NB cells.
methodsPublic datasets were used to predict the correlation of FGFR1 expression with NB clinical outcomes. Whole genome sequencing data of 19 paired diagnostic and relapse NB samples were used to find somatic mutations. In NB cell lines, silencing by short hairpin RNA and transient overexpression of FGFR1 were performed to evaluate the effect of the identified mutation by cell growth, invasion and cologenicity assays. HEK293, SHSY5Y and SKNBE2 were selected to investigate subcellular wild-type and mutated protein localization. FGFR1 inhibitor (AZD4547), alone or in combination with PI3K inhibitor (GDC0941), was used to rescue malignant phenotypes induced by overexpression of FGFR1 wild-type and mutated protein.
resultsHigh FGFR1 expression correlated with low relapse-free survival in two independent NB gene expression datasets. In addition, we found the somatic mutation N546K, the most recurrent point mutation of FGFR1 in all cancers and already reported in NB, in one out of 19 matched primary and recurrent tumors. Loss of FGFR1 function attenuated invasion and cologenicity in NB cells, whereas FGFR1 overexpression enhanced oncogenicity. The overexpression of FGFR1
conclusionsFGFR1 is an actionable driver oncogene in NB and a promising therapy may consist in targeting FGFR1 mutations in patients with therapy-resistant NB.
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