Evidence map›Paper›PMID 33235319›Full record

ArticleExperimental & molecular medicine2020

FGF401 and vinorelbine synergistically mediate antitumor activity and vascular normalization in FGF19-dependent hepatocellular carcinoma.

Hung Huynh, Aldo Prawira, Thi Bich Uyen Le, Thanh Chung Vu, Huai-Xiang Hao, Alan Huang, Youzhen Wang, Diana Graus Porta

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  6. Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Hung HuynhLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore, Singapore. cmrhth@nccs.com.sg.
Aldo PrawiraLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore, Singapore.ORCID http://orcid.org/0000-0003-4414-6928
Thi Bich Uyen LeLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore, Singapore.
Thanh Chung VuLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore, Singapore.
Huai-Xiang HaoOncology Drug Discovery Pharmacology, Novartis Institutes for Biomedical Research, 250 Massachusetts Avenue, Cambridge, MA, 02139, USA.
Alan HuangOncology Drug Discovery Pharmacology, Novartis Institutes for Biomedical Research, 250 Massachusetts Avenue, Cambridge, MA, 02139, USA.
Youzhen WangOncology Drug Discovery Pharmacology, Novartis Institutes for Biomedical Research, 250 Massachusetts Avenue, Cambridge, MA, 02139, USA.
Diana Graus PortaOncology Translational Research, Novartis Institutes for Biomedical Research at Basel, Basel, Switzerland.
National Cancer Centre Singapore · SGNovartis (Switzerland) · CH

Funding

MOH | National Medical Research Council (NMRC) NMRC/MOHIAFCat1/0009/2014MOH | National Medical Research Council (NMRC) NMRC/MOHIAFCat1/0026/2015National Research Foundation Singapore (National Research Foundation-Prime Minister's office, Republic of Singapore) NRF-CRP17-2017-05
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a lethal cancer with limited therapeutic options, and standard therapy with sorafenib provides only modest survival benefits. Fibroblast growth factor 19 (FGF19) has been proposed as a driver oncogene, and targeting its receptor, FGFR-4, may provide a better alternative to standard therapy for patients with FGF19-driven tumors. Sixty-three HCC patient-derived xenograft (PDX) models were screened for FGF19 expression. Mice bearing high and low FGF19-expressing tumors were treated with FGF401 and/or vinorelbine, and the antitumor activity of both agents was assessed individually and in combination. Tumor vasculature and intratumoral hypoxia were also examined. High FGF19 expression was detected in 14.3% (9 of 63) of the HCC models tested and may represent a good target for HCC treatment. FGF401 potently inhibited the growth of high FGF19-expressing HCC models regardless of FGF19 gene amplification. Furthermore, FGF401 inhibited the FGF19/FGFR-4 signaling pathway, cell proliferation, and hypoxia, induced apoptosis and blood vessel normalization and prolonged the overall survival (OS) of mice bearing high FGF19 tumors. FGF401 synergistically acted with the microtubule-depolymerizing drug vinorelbine to further suppress tumor growth, promote apoptosis, and prolong the OS of mice bearing high FGF19 tumors, with no evidence of increased toxicity. Our study suggests that a subset of patients with high FGF19-expressing HCC tumors could benefit from FGF401 or FGF401/vinorelbine treatment. A high level of FGF19 in a tumor may serve as a potential biomarker for patient selection.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicApoptosisCarcinoma, HepatocellularCell CycleCell Line, TumorCell ProliferationDisease Models, AnimalDrug SynergismFibroblast Growth FactorsGene ExpressionHumansImmunohistochemistryLiver NeoplasmsMicePiperazinesAntineoplastic Agents, PhytogenicFGF19 protein, humanFGFR4 protein, humanFibroblast Growth FactorsPiperazinesPyridinesReceptor, Fibroblast Growth Factor, Type 4roblitinibVinorelbine

Identifiers

PMID33235319
PMCPMC8080677
OpenAlexW3107321081

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.