Evidence map›Paper›PMID 15990860›Full record

ArticleLeukemia2005

Induction of centrosome and chromosome aberrations by imatinib in vitro.

A Fabarius, M Giehl, O Frank, P Duesberg, A Hochhaus, R Hehlmann, W Seifarth

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-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.

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

21 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Evaluation of oxidative stress responses in human circulating blood cells after imatinib mesylate treatment - Implications to its mechanism of action.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2019
    Article
  4. Review
  5. Toxicity of the mixture of selected antineoplastic drugs against aquatic primary producers.Environmental science and pollution research international · 2016
    Article
  6. Analyses of combined effects of cytostatic drugs on micronucleus formation in the Tradescantia.Environmental science and pollution research international · 2016
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. A clinical overview of centrosome amplification in human cancers.International journal of biological sciences · 2011
    Review
  18. Chronic myeloid leukemia: mechanisms of blastic transformation.The Journal of clinical investigation · 2010
    Review
  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

7 authors at 3 institutions in 2 countries.

A FabariusIII. Medizinische Universitätsklinik, Fakultät für Klinische Medizin Mannheim der Ruprecht-Karls-Universität Heidelberg, Mannheim, Germany. alice.fabarius@med3.ma.uni-heidelberg.de
M Giehl
O Frank
P Duesberg
A Hochhaus
R Hehlmann
W Seifarth
University Hospital Heidelberg · DEHeidelberg University · DEUniversity of California, Berkeley · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Imatinib (STI571, Gleevec/Glivec) is a potent selective tyrosine kinase inhibitor and is used successfully in the treatment of chronic myeloid leukemia (CML). While karyotype alterations, in addition to the Philadelphia chromosome, are a common phenomenon of progressing CML, the observation of BCR-ABL-negative leukemic clones with distinct aberrant karyotypes under an imatinib regimen is not yet understood. Here we test the hypothesis that such tumor clones may be induced de novo from normal cells by imatinib. In vitro experiments with varying drug concentrations (5-20 microM) were performed on normal human dermal fibroblasts (NHDF), Chinese hamster embryonal and Indian muntjak fibroblasts. After 3 weeks of treatment, analysis of cell cultures by centrosome immunostaining and conventional cytogenetics revealed that imatinib induced centrosome and chromosome aberrations in all cultures in a significant dose-dependent and species-independent manner. Moreover, the results of NHDF long-term culture experiments demonstrated that aberrant phenotypes, emerging under imatinib treatment for 12 weeks, were not reversible after prolonged propagation omitting the drug. These observations suggest a causative role of imatinib in the origin of centrosome and karyotype aberrations (genetic instability) and thus may explain the emergence of clonal chromosomal abnormalities in BCR-ABL-negative progenitor cells under imatinib therapy.

Indexed as

AnimalsAntineoplastic AgentsBenzamidesCells, CulturedCentrosomeChromosome AberrationsCricetinaeCricetulusCytogenetic AnalysisDose-Response Relationship, DrugFibroblastsHumansImatinib MesylateIn Vitro TechniquesMuntjacsPiperazinesAntineoplastic AgentsBenzamidesImatinib MesylatePiperazinesPyrimidines

Identifiers

PMID15990860
OpenAlexW2106369839

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.