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Lee et al. Hepatoma Res 2018;4:52 Hepatoma Research
DOI: 10.20517/2394-5079.2018.42

Review Open Access

The fibroblast growth factor receptor pathway in
hepatocellular carcinoma

Joycelyn Jie Xin Lee, Su Pin Choo
Division of Medical Oncology, National Cancer Centre Singapore, 11 Hospital Drive, Singapore 169610, Singapore.

Correspondence to: Dr. Su Pin Choo, Division of Medical Oncology, National Cancer Centre Singapore, 11 Hospital Drive, Singapore
169610, Singapore. E-mail: choo.su.pin@singhealth.com.sg

How to cite this article: Lee JJX, Choo SP. The fibroblast growth factor receptor pathway in hepatocellular carcinoma. Hepatoma Res
2018;4:52. http://dx.doi.org/10.20517/2394-5079.2018.42

Received: 25 Apr 2018 First Decision: 19 Jun 2018 Revised: 2 Aug 2018 Accepted: 10 Aug 2018 Published: 13 Sep 2018

Science Editor: Guang-Wen Cao Copy Editor: Cai-Hong Wang Production Editor: Huan-Liang Wu

Abstract
Hepatocellular carcinoma is the third most common cause of cancer-related death globally and portends a poor
prognosis. The fibroblast growth factor receptor (FGFR) pathway is increasingly acknowledged to play a role in the
pathogenesis of hepatocellular carcinoma (HCC) and is postulated to be upregulated as a mechanism of resistance
to anti-VEGF treatment. We attempt to review the importance of the FGFR pathway in HCC oncogenesis, as well
as the current clinical evidence on the efficacy and safety of FGFR pathway inhibitors in HCC.

Keywords: Hepatocellular carcinoma, targeted therapy, fibroblast growth factor

INTRODUCTION
[1]
Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related death globally . Most
patients have advanced disease on diagnosis. In unresectable advanced disease, sorafenib used to be the only
available systemic therapy option available and prognosis was poor with a one-year survival rate of less than
[2]
50% .
[3]
HCC tumours harbour an average of 30-40 mutations, of which 20% may be driver mutations . The mo-
lecular complexity and heterogeneity of HCC likely underlies the reason for failure of multiple phase III
trials of targeted agents over the years. With improving technologies, we have been able to learn more about
the molecular mechanisms underlying the oncogenesis of HCC, and in recent past have seen breakthroughs
[4]
with several new drugs being added to our armamentarium both in the front-line and second-line setting ,
[5]
and many more compounds showing great promise on the horizon .

© The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
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