Evidence map›Paper›PMID 20072648›Full record

ArticleNeoplasia (New York, N.Y.)2010

An orally available small-molecule inhibitor of c-Met, PF-2341066, reduces tumor burden and metastasis in a preclinical model of ovarian cancer metastasis.

Marion Zillhardt, James G Christensen, Ernst Lengyel

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.5field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. A Phase I Trial of the MET/OncoTargets and therapy · 2021
    Trial
  3. Trial
  4. Trial
  5. Article
  6. Bioactive Products Targeting C-Met As Potential Antitumour Drugs.Anti-cancer agents in medicinal chemistry · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Regulation of HGF and c-MET Interaction in Normal Ovary and Ovarian Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2017
    Review
  15. Review
  16. Article
  17. OncoTargets and therapy · 2017
    Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Marion ZillhardtDepartment of Obstetrics, University of Chicago, Chicago, IL 60637, USA.
James G Christensen
Ernst Lengyel
University of Chicago · USPfizer (United States) · US

Funding

Multi-Disciplinary Training Grant in Cancer ResearchT32CA009594 · NCI · UNIVERSITY OF CHICAGO · PI KAY F MACLEOD, Scott A. Oakes · 1989 to 2026
$11.5M
Regulation of Adhesion and Proteolysis in Ovarian CancerR01CA111882 · NCI · UNIVERSITY OF CHICAGO · PI LENGYEL, ERNST · 2006 to 2016
$2.8M
NCI NIH HHS R01 CA111882NCI NIH HHS T32 CA009594Wellcome Trust
6 · The paper itself

Abstract

Deregulated expression of the hepatocyte growth factor (HGF) receptor, c-Met, in cancer contributes to tumor progression and metastasis. The objective of this study was to determine whether blocking c-Met with an orally available c-Met inhibitor, PF-2341066, reduces tumor burden and increases survival in a xenograft model of ovarian cancer metastasis. Treatment of mice injected interperitoneally with SKOV3ip1 cells showed reduced overall tumor burden. Tumor weight and the number of metastases were reduced by 55% (P < .0005) and 62% (P < .0001), respectively. Treatment also increased median survival from 45 to 62 days (P = .0003). In vitro, PF-2341066 reduced HGF-stimulated phosphorylation of c-Met in the tyrosine kinase domain as well as phosphorylation of the downstream signaling effectors, Akt and Erk. It was apparent that inhibition of the pathways was functionally important because HGF-induced branching morphogenesis was also inhibited. In addition, proliferation and adhesion to various extracellular matrices were inhibited by treatment with PF-2341066, and the activity of matrix metalloproteinases was decreased in tumor tissue from treated mice compared with those receiving vehicle. Overall, these data indicate that PF-2341066 effectively reduces tumor burden in an in vivo model of ovarian cancer metastasis and may be a good therapeutic candidate in the treatment of patients with ovarian cancer.

Indexed as

Xenograft Model Antitumor AssaysAnimalsApoptosisBlotting, WesternCell CycleCell Line, TumorCell ProliferationCrizotinibFemaleHepatocyte Growth FactorHumansImmunohistochemistryMiceMice, NudeMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3CrizotinibHepatocyte Growth FactorMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PiperidinesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metPyrazolesPyridines

Identifiers

PMID20072648
PMCPMC2805878
OpenAlexW1214944030

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.