Evidence map›Paper›PMID 25197268›Full record

ArticleCurrent signal transduction therapy2011

The Hepatocyte Growth Factor Receptor: Structure, Function and Pharmacological Targeting in Cancer.

Fabiola Cecchi, Daniel C Rabe, Donald P Bottaro

Abstract read
In one paragraph

Article in Current signal transduction therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.1field-weighted citation impact, top 46% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. AberrantCells · 2024
    Review
  7. Review
  8. Article
  9. Targeting MET in Non-Small Cell Lung Cancer (NSCLC): A New Old Story?International journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Discovery and Therapeutic Exploitation of Mechanisms of Resistance to MET Inhibitors in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  18. Review
  19. Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2017
    Article
  20. A Review of Anti-Angiogenic Targets for Monoclonal Antibody Cancer Therapy.International journal of molecular sciences · 2017
    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

3 authors at 3 institutions in 1 country.

Fabiola CecchiUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Daniel C RabeUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Donald P BottaroUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Center for Cancer Research · USNational Cancer Institute · USNational Institutes of Health · US

Funding

Oncogenic Met Signaling in Urologic MalignanciesZIABC011124 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BOTTARO, DONALD · 2009 to 2021
$5.8M
Oncogenic Met Signaling in Urologic MalignanciesZ01BC011124 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BOTTARO, DONALD · 2008 to 2008
$242k
Intramural NIH HHS Z01 BC011124
6 · The paper itself

Abstract

Under normal conditions, hepatocyte growth factor (HGF)-induced activation of its cell surface receptor, the Met tyrosine kinase (TK), is tightly regulated by paracrine ligand delivery, ligand activation at the target cell surface, and ligand activated receptor internalization and degradation. Despite these controls, HGF/Met signaling contributes to oncogenesis and tumor progression in several cancers and promotes aggressive cellular invasiveness that is strongly linked to tumor metastasis. The prevalence of HGF/Met pathway activation in human malignancies has driven rapid growth in cancer drug development programs. Pathway inhibitors can be divided broadly into biologicals and low molecular weight synthetic TK inhibitors; of these, the latter now outnumber all other inhibitor types. We review here Met structure and function, the basic properties of HGF/Met pathway antagonists now in preclinical and clinical development, as well as the latest clinical trial results. The main challenges facing the effective use of HGF/Met-targeted antagonists for cancer treatment include optimal patient selection, diagnostic and pharmacodynamic biomarker development, and the identification and testing of optimal therapy combinations. The wealth of basic information, analytical reagents and model systems available concerning HGF/Met oncogenic signaling will continue to be invaluable in meeting these challenges and moving expeditiously toward more effective disease control.

Indexed as

Hepatocyte growth factorMet

Identifiers

PMID25197268
PMCPMC4156285
OpenAlexW2075092141

What OpenQuestion holds

Textmetadata
LicenceTDM
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.