Evidence map›Paper›PMID 32429395›Full record

ArticleCancers2020

Feasibility of Targeting Traf2-and-Nck-Interacting Kinase in Synovial Sarcoma.

Tetsuya Sekita, Tesshi Yamada, Eisuke Kobayashi, Akihiko Yoshida, Toru Hirozane, Akira Kawai, Yuko Uno, Hideki Moriyama, Masaaki Sawa, Yuichi Nagakawa and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. American journal of physiology. Renal physiology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Structural Insight into TNIK Inhibition.International journal of molecular sciences · 2022
    Review
  11. Wnt/β-catenin signaling in cancers and targeted therapies.Signal transduction and targeted therapy · 2021
    Review
  12. 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

15 authors at 3 institutions in 1 country.

Tetsuya SekitaLaboratory of Collaborative Research, Division of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.ORCID 0000-0002-4000-6891
Tesshi YamadaDepartment of Gastrointestinal and Pediatric Surgery, Tokyo Medical University, Tokyo 160-0023, Japan.
Eisuke KobayashiDivision of Musculoskeletal Oncology, National Cancer Center Hospital, Tokyo 104-0045, Japan.
Akihiko YoshidaDepartment of Diagnostic Pathology, National Cancer Center Hospital, Tokyo 104-0045, Japan.
Toru HirozaneDepartment of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Akira KawaiDivision of Musculoskeletal Oncology, National Cancer Center Hospital, Tokyo 104-0045, Japan.
Yuko UnoCarna Biosciences, Inc., Kobe 650-0047, Japan.
Hideki MoriyamaCarna Biosciences, Inc., Kobe 650-0047, Japan.
Masaaki SawaCarna Biosciences, Inc., Kobe 650-0047, Japan.
Yuichi NagakawaDepartment of Gastrointestinal and Pediatric Surgery, Tokyo Medical University, Tokyo 160-0023, Japan.
Akihiko TsuchidaDepartment of Gastrointestinal and Pediatric Surgery, Tokyo Medical University, Tokyo 160-0023, Japan.
Morio MatsumotoDepartment of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Masaya NakamuraDepartment of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Robert NakayamaDepartment of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Mari MasudaLaboratory of Collaborative Research, Division of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.ORCID 0000-0003-2311-8696
Keio University · JPTokyo Medical University · JPTokyo National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe treatment of patients with metastatic synovial sarcoma is still challenging, and the development of new molecular therapeutics is desirable. Dysregulation of Wnt signaling has been implicated in synovial sarcoma. Traf2-and-Nck-interacting kinase (TNIK) is an essential transcriptional co-regulator of Wnt target genes. We examined the efficacy of a small interfering RNA (siRNA) to

methodsThe expression of TNIK was determined in 20 clinical samples of synovial sarcoma. The efficacy of NCB-0846 was evaluated in four synovial sarcoma cell lines and a mouse xenograft model.

resultsWe found that synovial sarcoma cell lines with Wnt activation were highly dependent upon the expression of DISCUSSION: It has become evident that activation of Wnt signaling is causatively involved in the pathogenesis of synovial sarcoma, but no molecular therapeutics targeting the pathway have been approved. This study revealed for the first time the therapeutic potential of TNIK inhibition in synovial sarcoma.

Indexed as

MYCNCB-0846synovial sarcomaTNIKWnt signaling

Identifiers

PMID32429395
PMCPMC7281028
OpenAlexW3025414161

What OpenQuestion holds

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LicenceCC BY
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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.