Evidence map›Paper›PMID 20946682›Full record

ArticleBMC cancer2010

Efficacy of c-Met inhibitor for advanced prostate cancer.

William H Tu, Chunfang Zhu, Curtis Clark, James G Christensen, Zijie Sun

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. A Phase I Trial of the MET/OncoTargets and therapy · 2021
    Trial
  2. Review
  3. Article
  4. Article
  5. eLife · 2023
    Article
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  7. Review
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  16. Article
  17. Review
  18. Novel bone-targeting agents in prostate cancer.Prostate cancer and prostatic diseases · 2014
    Review
  19. Cabozantinib inhibits prostate cancer growth and prevents tumor-induced bone lesions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    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

5 authors at 2 institutions in 1 country.

William H TuDepartment of Urology, Stanford University School of Medicine, Stanford, CA 94305-5328, USA. wtu1@stanford.edu
Chunfang Zhu
Curtis Clark
James G Christensen
Zijie Sun
Stanford University · USPfizer (United States) · US

Funding

Roles of the androgen receptor and its co-regulators in prostate tumorigenesisR01CA070297 · NCI · STANFORD UNIVERSITY · PI SUN, ZIJIE · 2003 to 2025
$5.0M
ANDROGEN RECEPTOR ASSOCIATED PROTEINS IN PROSTATE CANCERR29CA070297 · NCI · STANFORD UNIVERSITY · PI SUN, ZIJIE · 1997 to 2002
$329k
NCI NIH HHS CA70297NCI NIH HHS R01 CA070297
6 · The paper itself

Abstract

backgroundAberrant expression of HGF/SF and its receptor, c-Met, often correlates with advanced prostate cancer. Our previous study showed that expression of c-Met in prostate cancer cells was increased after attenuation of androgen receptor (AR) signalling. This suggested that current androgen ablation therapy for prostate cancer activates c-Met expression and may contribute to development of more aggressive, castration resistant prostate cancer (CRPC). Therefore, we directly assessed the efficacy of c-Met inhibition during androgen ablation on the growth and progression of prostate cancer.

methodsWe tested two c-Met small molecule inhibitors, PHA-665752 and PF-2341066, for anti-proliferative activity by MTS assay and cell proliferation assay on human prostate cancer cell lines with different levels of androgen sensitivity. We also used renal subcapsular and castrated orthotopic xenograft mouse models to assess the effect of the inhibitors on prostate tumor formation and progression.

resultsWe demonstrated a dose-dependent inhibitory effect of PHA-665752 and PF-2341066 on the proliferation of human prostate cancer cells and the phosphorylation of c-Met. The effect on cell proliferation was stronger in androgen insensitive cells. The c-Met inhibitor, PF-2341066, significantly reduced growth of prostate tumor cells in the renal subcapsular mouse model and the castrated orthotopic mouse model. The effect on cell proliferation was greater following castration.

conclusionsThe c-Met inhibitors demonstrated anti-proliferative efficacy when combined with androgen ablation therapy for advanced prostate cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell Line, TumorCrizotinibDisease Models, AnimalDrug Screening Assays, AntitumorHumansIndolesMaleMiceNeoplasm TransplantationPhosphorylationPiperidinesProstatic NeoplasmsProto-Oncogene Proteins c-metPyrazoles5-((2,6-dichlorobenzyl)sulfonyl)-3-((3,5-dimethyl-4-((2-(pyrrolidin-1-ylmethyl)pyrrolidin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-1,3-dihydro-2H-indol-2-oneCrizotinibIndolesPiperidinesProto-Oncogene Proteins c-metPyrazolesPyridinesSulfones

Identifiers

PMID20946682
PMCPMC2964640
OpenAlexW2130040381

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.