Evidence map›Paper›PMID 28946903›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

High expression of Bruton's tyrosine kinase (BTK) is required for EGFR-induced NF-κB activation and predicts poor prognosis in human glioma.

Chenglong Yue, Mingshan Niu, Qian Qian Shan, Ting Zhou, Yiming Tu, Peng Xie, Lei Hua, Rutong Yu, Xuejiao Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Review
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  10. BTK, the new kid on the (oncology) block?Frontiers in oncology · 2022
    Review
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  17. p65BTK Is a Novel Biomarker and Therapeutic Target in Solid Tumors.Frontiers in cell and developmental biology · 2021
    Review
  18. 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

9 authors at 2 institutions in 1 country.

Chenglong YueInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Mingshan NiuBlood Diseases Institute, Jiangsu Key Laboratory of Bone Marrow Stem Cell, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Qian Qian ShanInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Ting ZhouDepartment of Gastroenterology, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Yiming TuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Peng XieDepartment of Neurosurgery, Huai'an Hospital Affiliated of Xuzhou Medical University and Huai'an Second People's Hospital, Huaian, Jiangsu, China.
Lei HuaBrain Hospital, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.
Rutong YuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, China. yu.rutong@163.com.
Xuejiao LiuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, China. liuxuejiao0923@126.com.
Xuzhou Medical College · CNSecond People’s Hospital of Huai’an · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMalignant glioma is the most common primary brain tumor in adults and has a poor prognosis. However, there are no effective targeted therapies for glioma patients. Thus, the development of novel targeted therapeutics for glioma is urgently needed.

methodsIn this study, we examined the prognostic significance BTK expression in patients with glioma. Furthermore, we investigated the mechanism and therapeutic potential of ibrutinib in the treatment of human glioma in vitro and in vivo.

resultsOur data demonstrate that high expression of BTK is a novel prognostic marker for poor survival in patients with glioma. BTK-specific inhibitor ibrutinib effectively inhibits the proliferation, migration and invasion ability of glioma cells. Furthermore, ibrutinib can induce G1 cell-cycle arrest by regulating multiple cell cycle-associated proteins. More importantly, we found that BTK inhibition significantly blocks the degradation of IκBα and prevents the nuclear accumulation of NF-κB p65 subunit induced by EGF in glioma cells.

conclusionsTaken together, our study suggests that BTK is a novel prognostic marker and molecular therapeutic target for glioma. BTK is required for EGFR-induced NF-κB activation in glioma cells. These findings provide the basis for future clinical studies of ibrutinib for the treatment of glioma.

Indexed as

Up-RegulationAdenineAgammaglobulinaemia Tyrosine KinaseAnimalsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationErbB ReceptorsGene Expression Regulation, NeoplasticGliomaHumansMiceNeoplasm TransplantationNF-kappa BPiperidinesAdenineAgammaglobulinaemia Tyrosine KinaseBTK protein, humanBtk protein, mouseEGFR protein, humanErbB ReceptorsibrutinibNF-kappa BPiperidinesProtein-Tyrosine KinasesPyrazolesPyrimidinesBTKClinical outcomeGliomaIbrutinibNF-κB pathway

Identifiers

PMID28946903
PMCPMC5613332
OpenAlexW2760407955

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Registered trials

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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.