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Fibroblast growth factor family as a potential target in the treatment of hepatocellular carcinoma

Authors Coleman S, Grose R, Kocher H

Received 25 February 2014

Accepted for publication 9 April 2014

Published 29 May 2014 Volume 2014:1 Pages 43—54

DOI https://doi.org/10.2147/JHC.S48958

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 5


Stacey J Coleman,1 Richard P Grose,1 Hemant M Kocher1,2

1Centre for Tumour Biology, Barts Cancer Institute – a CRUK Centre of Excellence, Queen Mary University of London, 2Barts and the London HPB Centre, The Royal London Hospital, Barts Health NHS Trust, London, UK

Abstract: Hepatocellular cancer (HCC) is currently the third leading cause of cancer death worldwide. The prognosis of patients diagnosed with late-stage disease is dismal due to high resistance to conventional systemic therapies. The introduction of sorafenib, despite its limited efficacy, as the standard systemic therapy for advanced HCC has paved a way for targeted molecular therapies for HCC. Fibroblast growth factor (FGF) signaling plays an important role in the developing embryo and the adult. The FGF signaling pathway is often hijacked by cancer cells, including HCC. Several alterations in FGF signaling correlate with poor outcome in HCC patients, suggesting that this family of signaling molecules plays an important role in the development of HCC. Multikinase inhibitors targeting FGF signaling are currently under investigation in clinical trials. This review discusses the current understanding of the biological and clinical implications of aberrant FGF signaling in the prognosis, diagnosis, and treatment of HCC.

Keywords: signaling, stroma, stellate, tumor, cross-talk


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