Evidence map›Paper›PMID 7708684›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Selective inhibition of the platelet-derived growth factor signal transduction pathway by a protein-tyrosine kinase inhibitor of the 2-phenylaminopyrimidine class.

E Buchdunger, J Zimmermann, H Mett, T Meyer, M Müller, U Regenass, N B Lydon

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 269 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Use of multitarget tyrosine kinase inhibitors to attenuate platelet-derived growth factor signalling in lung disease.European respiratory review : an official journal of the European Respiratory Society · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Immunological off-target effects of imatinib.Nature reviews. Clinical oncology · 2016
    Review
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  16. Article
  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

E BuchdungerCIBA Pharmaceuticals Division, Oncology Research Department, CIBA-Geigy Limited, Basel, Switzerland.
J Zimmermann
H Mett
T Meyer
M Müller
U Regenass
N B Lydon
Novartis (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The platelet-derived growth factor (PDGF) receptor is a member of the transmembrane growth factor receptor protein family with intrinsic protein-tyrosine kinase activity. We describe a potent protein-tyrosine kinase inhibitor (CGP 53716) that shows selectivity for the PDGF receptor in vitro and in the cell. The compound shows selectivity for inhibition of PDGF-mediated events such as PDGF receptor autophosphorylation, cellular tyrosine phosphorylation, and c-fos mRNA induction in response to PDGF stimulation of intact cells. In contrast, ligand-induced autophosphorylation of the epidermal growth factor (EGF) receptor, insulin receptor, and the insulin-like growth factor I receptor, as well as c-fos mRNA expression induced by EGF, fibroblast growth factor, and phorbol ester, was insensitive to inhibition by CGP 53716. In antiproliferative assays, the compound was approximately 30-fold more potent in inhibiting PDGF-mediated growth of v-sis-transformed BALB/c 3T3 cells relative to inhibition of EGF-dependent BALB/Mk cells, interleukin-3-dependent FDC-P1 cells, and the T24 bladder carcinoma line. When tested in vivo using highly tumorigenic v-sis- and human c-sis-transformed BALB/c 3T3 cells, CGP 53716 showed antitumor activity at well-tolerated doses. In contrast, CGP 53716 did not show antitumor activity against xenografts of the A431 tumor, which overexpresses the EGF receptor. These findings suggest that CGP 53716 may have therapeutic potential for the treatment of diseases involving abnormal cellular proliferation induced by PDGF receptor activation.

Indexed as

Protein Kinase Inhibitors3T3 CellsAnimalsAntineoplastic AgentsCarcinoma, Squamous CellCell DivisionCell LineCell Line, TransformedEpidermal Growth FactorFemaleFibroblast Growth Factor 2HumansKineticsMiceMice, Inbred BALB CMice, NudeAntineoplastic AgentsCGP 53716Epidermal Growth FactorFibroblast Growth Factor 2Oncogene Proteins v-sisPlatelet-Derived Growth FactorProtein Kinase InhibitorsProtein-Tyrosine KinasesPyridinesPyrimidinesReceptors, Platelet-Derived Growth FactorRetroviridae Proteins, OncogenicTetradecanoylphorbol Acetate

Identifiers

PMID7708684
PMCPMC42257
OpenAlexW2050596106

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.