Evidence map›Paper›PMID 28064454›Full record

ReviewCancer science2017

Hepatocyte growth factor/MET in cancer progression and biomarker discovery.

Kunio Matsumoto, Masataka Umitsu, Dinuka M De Silva, Arpita Roy, Donald P Bottaro

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 2 pooled it
13.0field-weighted citation impact, top 1% 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

143 citing papers in PubMed, 2 syntheses or guidelines pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026
    Review
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83 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 2 countries.

Kunio MatsumotoDivision of Tumor Dynamics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Masataka UmitsuLaboratory of Protein Synthesis and Expression, Institute for Protein Research, Osaka University, Osaka, Japan.
Dinuka M De SilvaUrologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Arpita RoyUrologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Donald P BottaroUrologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · USKanazawa University · JPNational Cancer Institute · USOsaka University · JP

Funding

Oncogenic Met Signaling in Urologic MalignanciesZIABC011124 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BOTTARO, DONALD · 2009 to 2021
$5.8M
6 · The paper itself

Abstract

Signaling driven by hepatocyte growth factor (HGF) and MET receptor facilitates conspicuous biological responses such as epithelial cell migration, 3-D morphogenesis, and survival. The dynamic migration and promotion of cell survival induced by MET activation are bases for invasion-metastasis and resistance, respectively, against targeted drugs in cancers. Recent studies indicated that MET in tumor-derived exosomes facilitates metastatic niche formation and metastasis in malignant melanoma. In lung cancer, gene amplification-induced MET activation and ligand-dependent MET activation in an autocrine/paracrine manner are causes for resistance to epidermal growth factor receptor tyrosine kinase inhibitors and anaplastic lymphoma kinase inhibitors. Hepatocyte growth factor secreted in the tumor microenvironment contributes to the innate and acquired resistance to RAF inhibitors. Changes in serum/plasma HGF, soluble MET (sMET), and phospho-MET have been confirmed to be associated with disease progression, metastasis, therapy response, and survival. Higher serum/plasma HGF levels are associated with therapy resistance and/or metastasis, while lower HGF levels are associated with progression-free survival and overall survival after treatment with targeted drugs in lung cancer, gastric cancer, colon cancer, and malignant melanoma. Urinary sMET levels in patients with bladder cancer are higher than those in patients without bladder cancer and associated with disease progression. Some of the multi-kinase inhibitors that target MET have received regulatory approval, whereas none of the selective HGF-MET inhibitors have shown efficacy in phase III clinical trials. Validation of the HGF-MET pathway as a critical driver in cancer development/progression and utilization of appropriate biomarkers are key to development and approval of HGF-MET inhibitors for clinical use.

Indexed as

Anaplastic Lymphoma KinaseBiomarkers, TumorCell MovementCell SurvivalDrug Resistance, NeoplasmEnzyme ActivationEpithelial CellsErbB ReceptorsHepatocyte Growth FactorHumansNeoplasm MetastasisNeoplasmsProto-Oncogene Proteins c-metReceptor Protein-Tyrosine KinasesSignal TransductionTumor MicroenvironmentALK protein, humanAnaplastic Lymphoma KinaseBiomarkers, TumorEGFR protein, humanErbB ReceptorsHepatocyte Growth FactorHGF protein, humanProto-Oncogene Proteins c-metReceptor Protein-Tyrosine KinasesBiomarkerdrug resistanceHGFMETreceptor tyrosine kinase

Identifiers

PMID28064454
PMCPMC5378267
OpenAlexW2570649392

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.