Evidence map›Paper›PMID 17909624›Full record

ArticleThe Journal of clinical investigation2007

Why targeted therapy hasn't worked in advanced cancer.

Jack L Arbiser

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  3. Article
  4. Article
  5. Novel antiangiogenic agents in dermatology.Archives of biochemistry and biophysics · 2011
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Jack L ArbiserDepartment of Dermatology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia, USA. jarbise@emory.edu
Emory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this issue of the JCI, Nissen et al. report that a reciprocal interaction exists between the growth factors FGF2 and PDGF-BB, causing tumors to exhibit increased angiogenesis and metastatic potential. Both FGF2 and PDGF-BB signal through tyrosine kinase receptors, which have been the target of tyrosine kinase inhibitors for cancer therapies. These inhibitors are usually small molecules that inhibit the kinase activity of a receptor or nonreceptor tyrosine kinase, preventing downstream signaling. The results of this study shed light on why tyrosine kinase inhibitors have been useful for the treatment of only a small number of advanced cancers. Currently, a major focus of pharmaceutical companies is to develop ever more potent and specific tyrosine kinases. The results presented here suggest that this approach may not be successful.

Indexed as

BecaplerminFibroblast Growth Factor 2HumansNeoplasmsPlatelet-Derived Growth FactorProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-sisSignal TransductionTreatment OutcomeBecaplerminFibroblast Growth Factor 2Platelet-Derived Growth FactorProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-sis

Identifiers

PMID17909624
PMCPMC1994633
OpenAlexW2002564810

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.