Evidence map›Paper›PMID 28420162›Full record

ReviewCancers2017

Hepatocyte Growth Factor, a Key Tumor-Promoting Factor in the Tumor Microenvironment.

Benjamin Yaw Owusu, Robert Galemmo, James Janetka, Lidija Klampfer

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

81 citing papers in PubMed, 123 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Progress in Designing Cytokine Antagonist Antibodies for Cancer Therapy.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
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  15. Profibrinolytic Factors and Cancer Progression, Metastasis, and Survival.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

21 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

4 authors at 2 institutions in 1 country.

Benjamin Yaw OwusuDepartment of Oncology, Drug Discovery Division, Southern Research Institute, Birmingham, AL 35205, USA. bnyowusu@uab.edu.
Robert GalemmoProtexase Therapeutics, St. Louis, MO 63110, USA. galemmo@protexase.com.
James JanetkaDepartment of Biochemistry and Molecular Biophysics, Alvin J. Siteman Cancer Center, Washington University in St. Louis, St. Louis, MO 63110, USA. janetkaj@wustl.edu.
Lidija KlampferDepartment of Oncology, Drug Discovery Division, Southern Research Institute, Birmingham, AL 35205, USA. klampfer@southernresearch.org.
Southern Research Institute · USWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor microenvironment plays a key role in tumor development and progression. Stromal cells secrete growth factors, cytokines and extracellular matrix proteins which promote growth, survival and metastatic spread of cancer cells. Fibroblasts are the predominant constituent of the tumor stroma and Hepatocyte Growth Factor (HGF), the specific ligand for the tyrosine kinase receptor c-MET, is a major component of their secretome. Indeed, cancer-associated fibroblasts have been shown to promote growth, survival and migration of cancer cells in an HGF-dependent manner. Fibroblasts also confer resistance to anti-cancer therapy through HGF-induced epithelial mesenchymal transition (EMT) and activation of pro-survival signaling pathways such as ERK and AKT in tumor cells. Constitutive HGF/MET signaling in cancer cells is associated with increased tumor aggressiveness and predicts poor outcome in cancer patients. Due to its role in tumor progression and therapeutic resistance, both HGF and MET have emerged as valid therapeutic targets. Several inhibitors of MET and HGF are currently being tested in clinical trials. Preclinical data provide a strong indication that inhibitors of HGF/MET signaling overcome both primary and acquired resistance to EGFR, HER2, and BRAF targeting agents. These findings support the notion that co-targeting of cancer cells and stromal cells is required to prevent therapeutic resistance and to increase the overall survival rate of cancer patients. HGF dependence has emerged as a hallmark of therapeutic resistance, suggesting that inhibitors of biological activity of HGF should be included into therapeutic regimens of cancer patients.

Indexed as

fibroblastsHGFtumor microenvironment

Identifiers

PMID28420162
PMCPMC5406710
OpenAlexW2605963676

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.