Targeting the fibroblast growth factor receptor family in cancer

Highlights • Deregulation of the FGF/FGFR signalling axis is observed in a wide variety of human carcinomas. • FGFR and EGFR pathways offer a compensatory signalling escape mechanism when either is inhibited. • Co-activation of c-MET and FGFR has been observed in several cancer cell lines • Dual FGF...

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Bibliographic Details
Published in:Cancer treatment reviews 2016-05, Vol.46, p.51-62
Main Authors: Hallinan, Niamh, Finn, Stephen, Cuffe, Sinead, Rafee, Shereen, O’Byrne, Kenneth, Gately, Kathy
Format: Article
Language:English
Subjects:
Animals
Antineoplastic Agents - pharmacology
Antineoplastic Agents - therapeutic use
EGFR
FGF ligand
FGFR
Fibroblast Growth Factors - antagonists & inhibitors
Fibroblast Growth Factors - metabolism
Hematology, Oncology and Palliative Medicine
Humans
Molecular Targeted Therapy
Neoplasms - drug therapy
Neoplasms - enzymology
Neoplasms - metabolism
Protein Kinase Inhibitors - pharmacology
Protein Kinase Inhibitors - therapeutic use
Receptor tyrosine kinase
Receptors, Fibroblast Growth Factor - antagonists & inhibitors
Receptors, Fibroblast Growth Factor - metabolism
Signal Transduction
Targeted therapy
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Summary:Highlights • Deregulation of the FGF/FGFR signalling axis is observed in a wide variety of human carcinomas. • FGFR and EGFR pathways offer a compensatory signalling escape mechanism when either is inhibited. • Co-activation of c-MET and FGFR has been observed in several cancer cell lines • Dual FGFR kinase targeting inhibitors such as FIIN-3 may be able to overcome clinical resistance. • Co-targeting FGFR pathway and a parallel proliferative pathway may overcome clinical resistance.
ISSN:0305-7372
1532-1967
DOI:10.1016/j.ctrv.2016.03.015