Varaico: Literature-Extracted Genetic Variants

Gene:FGFR4
Variant:p.V550E
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FGFR4

NM_213647.3:p.V550E

Associated Papers

Genomic Profiling of Pediatric Solid Tumors With a Dual DNA/RNA Panel: JCCG-TOP2 Study.

Tao K et al.

Cancer Science, 2026

Saturation mutagenesis identifies activating and resistance-inducing FGFR kinase domain mutations.

Tangermann C et al.

Nature Genetics, 2026

41361008 (PubMed )
Supplement: 41588_2025_2431_MOESM6_ESM.xlsx › Figure_E5f

Therapeutic advances of targeting receptor tyrosine kinases in cancer.

Tomuleasa C et al.

Signal Transduction and Targeted Therapy, 2024

Germline variants in patients diagnosed with pediatric soft tissue sarcoma.

Yndestad S et al.

Acta Oncologica (stockholm, Sweden), 2024

39037077 (PubMed )
Supplement: AO-63-40730-s1.xlsx › 3-Somatic_variants

A biobank of pediatric patient-derived-xenograft models in cancer precision medicine trial MAPPYACTS for relapsed and refractory tumors.

Marques Da Costa ME et al.

Communications Biology, 2023

37723198 (PubMed )
Supplement: 42003_2023_5320_MOESM4_ESM.xlsx › Suppl._Data_1

Biological and clinical implications of FGFR aberrations in paediatric and young adult cancers.

Brown LM et al.

Oncogene, 2023

Gatekeeper mutations activate FGF receptor tyrosine kinases by destabilizing the autoinhibited state.

Besch A et al.

Proceedings of the National Academy of Sciences of the United States of America, 2023

The clinical utility of integrative genomics in childhood cancer extends beyond targetable mutations.

Villani A et al.

Nature Cancer, 2023

36585449 (PubMed )
Supplement: 43018_2022_474_MOESM10_ESM.xlsx › Table_S5_-_Category_C_variants

Strategies to inhibit FGFR4 V550L-driven rhabdomyosarcoma.

Fiorito E et al.

British Journal of Cancer, 2022

Molecularly Targeted Therapy towards Genetic Alterations in Advanced Bladder Cancer.

Thomas J et al.

Cancers, 2022

Targeted therapies: Expanding the role of FGFR3 inhibition in urothelial carcinoma.

Zengin ZB et al.

Urologic Oncology, 2022

Discovery of AS-1763: A Potent, Selective, Noncovalent, and Orally Available Inhibitor of Bruton's Tyrosine Kinase.

Kawahata W et al.

Journal of Medicinal Chemistry, 2021

34529443 (PubMed )
Supplement: jm1c01279_si_001.pdf

Molecular mechanisms of the anti-cancer drug, LY2874455, in overcoming the FGFR4 mutation-based resistance.

Dehghanian F et al.

Scientific Reports, 2021

Fibroblast growth factor receptors in cancer: genetic alterations, diagnostics, therapeutic targets and mechanisms of resistance.

Krook MA et al.

British Journal of Cancer, 2021

FGFR4 Gly388Arg Polymorphism Reveals a Poor Prognosis, Especially in Asian Cancer Patients: A Meta-Analysis.

Kim JH et al.

Frontiers in Oncology, 2021

Therapeutics potentiating microglial p21-Nrf2 axis can rescue neurodegeneration caused by neuroinflammation.

Nakano-Kobayashi A et al.

Science Advances, 2020

33188020 (PubMed )
Supplement: abc1428_SM.pdf

FGFR4: A promising therapeutic target for breast cancer and other solid tumors.

Levine KM et al.

Pharmacology & Therapeutics, 2020

Identification of a novel oncogenic mutation of FGFR4 in gastric cancer.

Futami T et al.

Scientific Reports, 2019

Insight into ponatinib resistance mechanisms in rhabdomyosarcoma caused by the mutations in FGFR4 tyrosine kinase using molecular modeling strategies.

Wu C et al.

International Journal of Biological Macromolecules, 2019

The FGFR1 V561M Gatekeeper Mutation Drives AZD4547 Resistance through STAT3 Activation and EMT.

Ryan MR et al.

Molecular Cancer Research : Mcr, 2019

Functional screening of FGFR4-driven tumorigenesis identifies PI3K/mTOR inhibition as a therapeutic strategy in rhabdomyosarcoma.

McKinnon T et al.

Oncogene, 2018

Inhibitor repurposing reveals ALK, LTK, FGFR, RET and TRK kinases as the targets of AZD1480.

Gudernova I et al.

Oncotarget, 2017

Landscape of activating cancer mutations in FGFR kinases and their differential responses to inhibitors in clinical use.

Patani H et al.

Oncotarget, 2016

Antitumor effects and molecular mechanisms of ponatinib on endometrial cancer cells harboring activating FGFR2 mutations.

Kim DH et al.

Cancer Biology & Therapy, 2016

Crystal Structure of the FGFR4/LY2874455 Complex Reveals Insights into the Pan-FGFR Selectivity of LY2874455.

Wu D et al.

Plos One, 2016

Integrative Clinical Sequencing in the Management of Refractory or Relapsed Cancer in Youth.

Mody RJ et al.

Jama, 2015

DFG-out mode of inhibition by an irreversible type-1 inhibitor capable of overcoming gate-keeper mutations in FGF receptors.

Huang Z et al.

Acs Chemical Biology, 2015

Structural insights into FGFR kinase isoform selectivity: diverse binding modes of AZD4547 and ponatinib in complex with FGFR1 and FGFR4.

Tucker JA et al.

Structure (london, England : 1993), 2014

Structural analysis of the human fibroblast growth factor receptor 4 kinase.

Lesca E et al.

Journal of Molecular Biology, 2014

Comparison of the cancer gene targeting and biochemical selectivities of all targeted kinase inhibitors approved for clinical use.

Uitdehaag JC et al.

Plos One, 2014

24651269 (PubMed )
Supplement: pone.0092146.s014.xlsx › table_S6_kinase_panel_data

Targeting wild-type and mutationally activated FGFR4 in rhabdomyosarcoma with the inhibitor ponatinib (AP24534).

Li SQ et al.

Plos One, 2013

Functional analysis of receptor tyrosine kinase mutations in lung cancer identifies oncogenic extracellular domain mutations of ERBB2.

Greulich H et al.

Proceedings of the National Academy of Sciences of the United States of America, 2012

Targeting mutant fibroblast growth factor receptors in cancer.

Greulich H et al.

Trends in Molecular Medicine, 2011

Identification of FGFR4-activating mutations in human rhabdomyosarcomas that promote metastasis in xenotransplanted models.

Taylor JG et al.

The Journal of Clinical Investigation, 2009

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Regarding the variants extracted from papers and shown text snippets from research papers, the following holds: "Some rights reserved. This work permits non-commercial use, distribution and reproduction in any medium, provided the original author and source are credited."