Evidence map›Paper›PMID 22650230›Full record

ArticleThyroid : official journal of the American Thyroid Association2012

Imatinib enhances docetaxel-induced apoptosis through inhibition of nuclear factor-κB activation in anaplastic thyroid carcinoma cells.

EunSook Kim, Michiko Matsuse, Vladimir Saenko, Keiji Suzuki, Akira Ohtsuru, Norisato Mitsutake, Shunichi Yamashita

Open access · greenAbstract read
In one paragraph

Article in Thyroid : official journal of the American Thyroid Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Advances in targeted therapy for anaplastic thyroid carcinoma.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  6. Article
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  8. Review
  9. Article
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  12. Sorafenib and Quinacrine Target Anti-Apoptotic Protein MCL1: A Poor Prognostic Marker in Anaplastic Thyroid Cancer (ATC).Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  13. Article
  14. Article
  15. Article
  16. Update: the status of clinical trials with kinase inhibitors in thyroid cancer.The Journal of clinical endocrinology and metabolism · 2014
    Review
  17. Review
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.

EunSook KimDepartment of Radiation Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Michiko Matsuse
Vladimir Saenko
Keiji Suzuki
Akira Ohtsuru
Norisato Mitsutake
Shunichi Yamashita
Nagasaki University · JPUlsan College · KRNagasaki University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe previously reported the partial effectiveness of imatinib (also known as STI571, Glivec, or Gleevec) on anaplastic thyroid cancer (ATC) cells. Imatinib is a selective tyrosine kinase inhibitor that has been used for various types of cancer treatments. Recently, several reports have demonstrated that imatinib enhanced the sensitivity of cancer cells to other anticancer drugs. In this study, therefore, we investigated whether imatinib enhances the antitumor activity of docetaxel in ATC cells.

methodsTwo ATC cell lines, FRO and KTC-2, were treated with imatinib and/or docetaxel. Cell survival assay and flow cytometry for annexin V were used to assess the induction of apoptosis. Changes of pro- and antiapoptotic factors were determined by Western blot. Nuclear factor-κB (NF-κB) activity was measured by DNA-binding assay. Tumor growth was also investigated in vivo.

resultsThe combined treatment significantly enhanced apoptosis compared with single treatment. ATC cells themselves expressed high levels of antiapoptotic factors, X-linked inhibitor of apoptosis (XIAP), and survivin. The treatment with docetaxel alone further increased their expressions; however, the combined treatment blocked the inductions. Although imatinib alone had no effect on NF-κB background levels, combined treatment significantly suppressed the docetaxel-induced NF-κB activation. Further, the combined administration of the drugs also showed significantly greater inhibitory effect on tumor growth in mice xenograft model.

conclusionsImatinib enhanced antitumor activity of docetaxel in ATC cells. Docetaxel seemed to induce both pro- and antiapoptotic signaling pathways in ATC cells, and imatinib blocked the antiapoptotic signal. Thus, docetaxel combined with imatinib emerges as an attractive strategy for the treatment of ATC.

Indexed as

Antineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBenzamidesCarcinomaCell Line, TumorCell ProliferationCell SurvivalDocetaxelDrug SynergismHumansImatinib MesylateNF-kappa BPiperazinesPyrimidinesTaxoidsAntineoplastic AgentsBenzamidesDocetaxelImatinib MesylateNF-kappa BPiperazinesPyrimidinesTaxoids

Identifiers

PMID22650230
PMCPMC3387763
OpenAlexW2060641409

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.