Evidence map›Paper›PMID 16170366›Full record

ArticleOncogene2006

FMS receptor for M-CSF (CSF-1) is sensitive to the kinase inhibitor imatinib and mutation of Asp-802 to Val confers resistance.

J R Taylor, N Brownlow, J Domin, N J Dibb

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02303899 (A Phase II Study of the Combination of Gemcitabine and Imatinib Mesylate in Pemetrexed-pretreated Patients With Malignant Pleural Mesothelioma), which is not on this map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 10% 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.

NCT02303899 phase2completednot on this mapstarted 2014, after this paper: background citation

A Phase II Study of the Combination of Gemcitabine and Imatinib Mesylate in Pemetrexed-pretreated Patients With Malignant Pleural Mesothelioma

TypeinterventionalSponsorIstituto Clinico HumanitasRan2014 to 2017Enrolled22ConditionsMesothelioma, MalignantArmsGemcitabine, Imatinib mesylate
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Mcl-1 Protein and Viral Infections: A Narrative Review.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Immune cells in primary and metastatic gastrointestinal stromal tumors (GIST).International journal of clinical and experimental pathology · 2014
    Article
  13. Abl family kinases regulate FcγR-mediated phagocytosis in murine macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

4 authors at 2 institutions in 1 country.

J R TaylorInstitute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, London, UK.
N Brownlow
J Domin
N J Dibb
Hammersmith Hospital · GBImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kinase inhibitor imatinib is used in the treatment of chronic myeloid leukaemia, where it targets the intracellular Bcr-Abl tyrosine kinase, and gastrointestinal stromal tumours, where it targets either the KIT or PDGF tyrosine kinase receptors. Here, we report that imatinib is also an effective inhibitor of the closely related FMS receptor for macrophage colony stimulating factor and that mutation of Asp 802 of FMS to Val confers imatinib resistance. Imatinib readily reverted the transformed phenotype of haemopoietic and fibroblast cell lines that express the oncogene v-fms and also inhibited the growth of the Bacl.2F5 macrophage cell line. The cellular IC50 value of imatinib for FMS was similar to those for Bcr-Abl and KIT. Consequently, imatinib may also prove effective for the treatment of diseases whose progression is dependent upon macrophage-colony stimulating factor, this includes certain aspects of cancer and inflammation.

Indexed as

Drug Resistance, NeoplasmMutationAnimalsAntineoplastic AgentsAspartic AcidBenzamidesDisease ProgressionDose-Response Relationship, DrugDown-RegulationFusion Proteins, bcr-ablHumansImatinib MesylateInflammationInhibitory Concentration 50Macrophage Colony-Stimulating FactorMiceAntineoplastic AgentsAspartic AcidBenzamidesFusion Proteins, bcr-ablImatinib MesylateMacrophage Colony-Stimulating FactorOncogene Protein v-cblPiperazinesProto-Oncogene Proteins c-crkProto-Oncogene Proteins c-kitPyrimidinesReceptor, Macrophage Colony-Stimulating FactorReceptor Protein-Tyrosine KinasesValine

Identifiers

PMID16170366
OpenAlexW1964698497

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.