Evidence map›Paper›PMID 12824898›Full record

ReviewCancer science2003

NK4 (HGF-antagonist/angiogenesis inhibitor) in cancer biology and therapeutics.

Kunio Matsumoto, Toshikazu Nakamura

Open access · greenAbstract readReview
In one paragraph

Review in Cancer science, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 152 citations in OpenAlex.

  1. Article
  2. Article
  3. Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024
    Review
  4. Review
  5. Mesenchymal stem/stromal cells in cancer therapy.Journal of hematology & oncology · 2021
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Small molecule inhibitor of c-Met (PHA665752) suppresses the growth of ovarian cancer cells and reverses cisplatin resistance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  16. Review
  17. Article
  18. Review
  19. Targeting the hepatocyte growth factor-cMET axis in cancer therapy.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012
    Article
  20. Mesenchymal stem cells engineered for cancer therapy.Advanced drug delivery reviews · 2012
    Review
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

2 authors at 1 institution in 1 country.

Kunio MatsumotoDivision of Molecular Regenerative Medicine, Course of Advanced Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Toshikazu Nakamura
The University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invasion and subsequent establishment of metastasis are devastating events for patients with cancer, but past therapeutic approaches have paid relatively little attention to these important issues. Hepatocyte growth factor (HGF) and its receptor, the c-Met tyrosine kinase, play roles in cancer invasion and metastasis in a wide variety of tumor cells. Activation of the c-Met receptor integrates multiple signal transduction pathways involved in cell-cell and cell-matrix interactions, cellular migration, and breakdown of the extracellular scaffold. Paracrine activation of the c-Met receptor by stromal-derived HGF mediates tumor-stromal interactions that facilitate invasion and metastasis. Likewise, aberrant expression of the c-Met receptor and autocrine or mutational activation of c-Met receptor tyrosine kinase are closely associated with the progression of malignant tumors. Based on this background, NK4, a competitive antagonist of HGF-c-Met association was prepared so as to block cancer invasion and metastasis. NK4, an internal fragment of HGF, binds to but does not activate the c-Met receptor, thereby competitively antagonizing the biological activities of HGF. Unexpectedly, NK4 was subsequently shown to be an angiogenesis inhibitor as well, and this angioinhibitory activity is independent of its action as an HGF-antagonist. Importantly, NK4 protein or NK4 gene therapy have been shown to inhibit tumor invasion, metastasis and angiogenesis, effectively converting malignant tumors into benign tumors. Targeting tumor invasion-metastasis and angiogenesis with NK4 seems to have considerable therapeutic potential for cancer patients.

Indexed as

MitogensAngiogenesis InhibitorsAnimalsGenetic TherapyHepatocyte Growth FactorHumansNeoplasmsProto-Oncogene Proteins c-metAngiogenesis InhibitorsHepatocyte Growth FactorHGF protein, humanMitogensProto-Oncogene Proteins c-met

Identifiers

PMID12824898
PMCPMC11160298
OpenAlexW1989401198

What OpenQuestion holds

Textmetadata
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.