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ePoster Display

365P - The analysis of FGFR-gene family alterations in glioma

Date

16 Sep 2021

Session

ePoster Display

Topics

Tumour Site

Central Nervous System Malignancies

Presenters

yunqian Li

Citation

Annals of Oncology (2021) 32 (suppl_5): S516-S529. 10.1016/annonc/annonc674

Authors

Y. Li1, T. han2, W. sun2, Y. lu3, G. lu2, W. deng3, R. ding4, F. bu4

Author affiliations

  • 1 Department Of Neurooncology, The First Hospital of Jilin University, 130021 - Changchun/CN
  • 2 The Medical Department, Jiangsu Simcere Diagnostics Co., Ltd., Nanjing, China, 210000 - Nanjing/CN
  • 3 Department Of Biological Information, Jiangsu Simcere Diagnostics Co., Ltd., Nanjing, China, 210000 - Nanjing/CN
  • 4 The State Key Lab Of Translational Medicine And Innovative Drug Development, Jiangsu Simcere Diagnostics Co., Ltd., Nanjing, China, 210000 - Nanjing/CN

Resources

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Abstract 365P

Background

Fibroblast growth factor (FGFR) alterations are implicated across a range of solid tumors, promoting oncogenesis as a result of amplification, mutations, and structural variations. The FGFR gene family consists of four highly conserved transmembrane tyrosine kinase receptors (FGFR1–4). FGFR signaling influences angiogenesis and tumor cell migration, differentiation, proliferation, and survival. Recently, the cIMPACT-NOW released update 4 and update research, which considered FGFR alterations as a marker in brain tumor classification and prognosis. FGFR inhibitors have presented good clinical trial data in CNS tumors. Therefore, the features of FGFR-gene family alterations in Chinese gliomas are of great interest.

Methods

Tumor specimens from 993 glioma patients were analyzed using the 131-gene profiling. FGFR variants including mutations, amplification, and fusion were detected by following the standard operating procedure (SOP). The molecular characteristics, FGFR mutation types, and frequency were also evaluated.

Results

A total of 116 FGFR variants, including mutations, fusions, and gene amplification were identified. The majority of the FGFR variants were mutations (62.1%), amplification and fusion being observed in similar frequencies (17.2%, 20.7%). FGFR1 alterations were slightly more than in FGFR2-4. Interestingly, we observed more amplification events in FGFR1 (66.7%, 13/20), more fusion in FGFR3 (75%, 18/24), no amplification in FGFR2, only mutations in FGFR4. In addition to FGFR-TACC fusion, 4 novel FGFR fusions retaining the intact kinase domain were detected, including FGFR3-KCNB1, FGFR3-POC1A, FGFR2-CEACAM1 (Intergenic), FGFR3-WASF2 (Intergenic). FGFR variants were more common in IDH wild-type and H3 mutant than in IDH-mutant gliomas (P=0.003461, P=0.002304). Pathway enrichment (GO, KEGG) analysis was performed, revealed no significant differences between FGFR mutation and wild type.

Conclusions

We report the prevalence of FGFR variants was 9.1% in in Chinese glioma patients, including mutations, gene amplifications, and novel FGFR fusions. Moreover, targeting FGFR pathway in gliomas with FGFR alterations may be a therapeutic strategy.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

Y. Li.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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