Evidence map›Paper›PMID 33321903›Full record

ArticleInternational journal of molecular sciences2020

Bevacizumab Augments the Antitumor Efficacy of Infigratinib in Hepatocellular Carcinoma.

Thi Bich Uyen Le, Thanh Chung Vu, Rebecca Zhi Wen Ho, Aldo Prawira, Lingzhi Wang, Boon Cher Goh, Hung Huynh

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
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  9. Cellular based immunotherapy for primary liver cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
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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

7 authors at 3 institutions in 1 country.

Thi Bich Uyen LeDepartment of Haematology-Oncology, National University Health System, Singapore 119074, Singapore.
Thanh Chung VuLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore.
Rebecca Zhi Wen HoLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore.
Aldo PrawiraLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore.ORCID 0000-0003-4414-6928
Lingzhi WangDepartment of Haematology-Oncology, National University Health System, Singapore 119074, Singapore.
Boon Cher GohDepartment of Haematology-Oncology, National University Health System, Singapore 119074, Singapore.
Hung HuynhLaboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, Singapore 169610, Singapore.
National Cancer Centre Singapore · SGNational University Cancer Institute, Singapore · SGNational University Health System · SG

Funding

National Research Foundation Singapore NRF-CRP17-2017-05RIE2020 NCIS Centre Grant CGAug16M005Singapore National Medical Research Council NMRC/MOHIAFCAT2/006/2016
6 · The paper itself

Abstract

The fibroblast growth factor (FGF) signaling cascade is one of the key signaling pathways in hepatocellular carcinoma (HCC). FGF has been shown to augment vascular endothelial growth factor (VEGF)-mediated HCC development and angiogenesis, as well as to potentially lead to resistance to VEGF/VEGF receptor (VEGFR)-targeted agents. Thus, novel agents targeting FGF/FGF receptor (FGFR) signaling may enhance and/or overcome de novo or acquired resistance to VEGF-targeted agents in HCC. Mice bearing high- and low-FGFR tumors were treated with Infigratinib (i.e., a pan-FGFR kinase inhibitor) and/or Bevacizumab (i.e., an angiogenesis inhibitor). The antitumor activity of both agents was assessed individually or in combination. Tumor vasculature, intratumoral hypoxia, and downstream targets of FGFR signaling pathways were also investigated. Infigratinib, when combined with Bevacizumab, exerted a synergistic inhibitory effect on tumor growth, invasion, and lung metastasis, and it significantly improved the overall survival of mice bearing FGFR-dependent HCC. Infigratinib/Bevacizumab promoted apoptosis, inhibited cell proliferation concomitant with upregulation of p27, and reduction in the expression of FGFR2-4, p-FRS-2, p-ERK1/2, p-p70S6K/4EBP1, Cdc25C, survivin, p-Cdc2, and p-Rb. Combining Infigratinib/Bevacizumab may provide therapeutic benefits for a subpopulation of HCC patients with FGFR-dependent tumors. A high level of FGFR-2/3 may serve as a potential biomarker for patient selection to Infigratinib/Bevacizumab.

Indexed as

Adaptor Proteins, Signal TransducingAngiogenesis InhibitorsAnimalsAntineoplastic Agents, ImmunologicalApoptosisBevacizumabCarcinoma, Hepatocellularcdc25 PhosphatasesCell Cycle ProteinsCell Line, TumorCell ProliferationDrug SynergismExtracellular Signal-Regulated MAP KinasesLiver NeoplasmsMaleMiceAdaptor Proteins, Signal TransducingAngiogenesis InhibitorsAntineoplastic Agents, ImmunologicalBevacizumabCdc25c protein, mousecdc25 PhosphatasesCell Cycle ProteinsEif4ebp1 protein, mouseExtracellular Signal-Regulated MAP KinasesinfigratinibPhenylurea CompoundsPyrimidinesRibosomal Protein S6 Kinases, 70-kDaSurvivinangiogenesis inhibitorgrowth inhibitionhepatocellular carcinomahypoxiainvasionpan-FGFR inhibitorvessel normalization

Identifiers

PMID33321903
PMCPMC7764786
OpenAlexW3112416175

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.