Evidence map›Paper›PMID 18620091›Full record

ReviewAdvances in cancer research2008

Met-related receptor tyrosine kinase Ron in tumor growth and metastasis.

Purnima K Wagh, Belinda E Peace, Susan E Waltz

Abstract readReview
In one paragraph

Review in Advances in cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
49.5field-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

95 citing papers in PubMed, 151 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Genetic Influences in Cancer-Associated Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2023
    Review
  7. Article
  8. RON (Cancers · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

35 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

3 authors at 1 institution in 1 country.

Purnima K WaghDepartment of Surgery, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0558, USA.
Belinda E Peace
Susan E Waltz
University of Cincinnati Medical Center · US

Funding

Hepatocyte Growth Factor-like Protein ReceptorR01DK073552 · NIDDK · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E · 2005 to 2009
$1.5M
The Ron Receptor/Chemokine Axis in Prostate CancerR01CA125379 · NCI · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E · 2008 to 2012
$1.3M
NCI NIH HHS R01 CA125379NIDDK NIH HHS R01 DK073552
6 · The paper itself

Abstract

The Ron receptor is a member of the Met family of cell surface receptor tyrosine kinases and is primarily expressed on epithelial cells and macrophages. The biological response of Ron is mediated by binding of its ligand, hepatocyte growth factor-like protein/macrophage stimulating-protein (HGFL). HGFL is primarily synthesized and secreted from hepatocytes as an inactive precursor and is activated at the cell surface. Binding of HGFL to Ron activates Ron and leads to the induction of a variety of intracellular signaling cascades that leads to cellular growth, motility and invasion. Recent studies have documented Ron overexpression in a variety of human cancers including breast, colon, liver, pancreas, and bladder. Moreover, clinical studies have also shown that Ron overexpression is associated with both worse patient outcomes as well as metastasis. Forced overexpression of Ron in transgenic mice leads to tumorigenesis in both the lung and the mammary gland and is associated with metastatic dissemination. While Ron overexpression appears to be a hallmark of many human cancers, the mechanisms by which Ron induces tumorigenesis and metastasis are still unclear. Several strategies are currently being undertaken to inhibit Ron as a potential therapeutic target; current strategies include the use of Ron blocking proteins, small interfering RNA (siRNA), monoclonal antibodies, and small molecule inhibitors. In total, these data suggest that Ron is a critical factor in tumorigenesis and that inhibition of this protein, alone or in combination with current therapies, may prove beneficial in the treatment of cancer patients.

Indexed as

AnimalsCell Transformation, NeoplasticChromosome MappingDisease ProgressionGene Expression Regulation, NeoplasticGrowth and DevelopmentHepatocyte Growth FactorHumansInflammationMiceModels, BiologicalNeoplasm MetastasisNeoplasmsNeovascularization, PathologicProtein-Tyrosine KinasesProto-Oncogene ProteinsHepatocyte Growth Factormacrophage stimulating proteinProtein-Tyrosine KinasesProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRON protein

Identifiers

PMID18620091
PMCPMC4102433
OpenAlexW1542053886

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.