Evidence map›Paper›PMID 34645618›Full record

ArticleLife science alliance2021

Kinomics platform using GBM tissue identifies BTK as being associated with higher patient survival.

Sofian Al Shboul, Olimpia E Curran, Javier A Alfaro, Fiona Lickiss, Erisa Nita, Jacek Kowalski, Faris Naji, Rudolf Nenutil, Kathryn L Ball, Radovan Krejcir and 3 more

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

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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

13 authors at 6 institutions in 5 countries.

Sofian Al ShboulInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK s.alshboul@ed.ac.uk.ORCID 0000-0002-0455-4380
Olimpia E CurranDepartment of Neuropathology, Western General Hospital, Edinburgh, UK.
Javier A AlfaroInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Fiona LickissInternational Centre for Cancer Vaccine Science, University of Gdansk, Gdansk, Poland.
Erisa NitaInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Jacek KowalskiInternational Centre for Cancer Vaccine Science, University of Gdansk, Gdansk, Poland.
Faris NajiPamgene International BV, 's-Hertogenbosch, Netherlands.
Rudolf NenutilResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
Kathryn L BallInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.ORCID 0000-0002-0728-7169
Radovan KrejcirResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
Borivoj VojtesekResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.ORCID 0000-0001-6194-3705
Ted R HuppInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Paul M BrennanInstitute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK paul.brennan@ed.ac.uk.ORCID 0000-0002-7347-830X
Edinburgh Cancer Research · GBMasaryk Memorial Cancer Institute · CZUniversity of Gdańsk · PLHashemite University · JOPamGene (Netherlands) · NLWestern General Hospital · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C511599/1Biotechnology and Biological Sciences Research Council BB/J00751X/1
6 · The paper itself

Abstract

Better understanding of GBM signalling networks in-vivo would help develop more physiologically relevant ex vivo models to support therapeutic discovery. A "functional proteomics" screen was undertaken to measure the specific activity of a set of protein kinases in a two-step cell-free biochemical assay to define dominant kinase activities to identify potentially novel drug targets that may have been overlooked in studies interrogating GBM-derived cell lines. A dominant kinase activity derived from the tumour tissue, but not patient-derived GBM stem-like cell lines, was Bruton tyrosine kinase (BTK). We demonstrate that BTK is expressed in more than one cell type within GBM tissue; SOX2-positive cells, CD163-positive cells, CD68-positive cells, and an unidentified cell population which is SOX2-negative CD163-negative and/or CD68-negative. The data provide a strategy to better mimic GBM tissue ex vivo by reconstituting more physiologically heterogeneous cell co-culture models including BTK-positive/negative cancer and immune cells. These data also have implications for the design and/or interpretation of emerging clinical trials using BTK inhibitors because BTK expression within GBM tissue was linked to longer patient survival.

Indexed as

Signal TransductionAgammaglobulinaemia Tyrosine KinaseBrain NeoplasmsCell Line, TumorCell SurvivalCoculture TechniquesGlioblastomaHumansNeoplastic Stem CellsProteomeProteomicsSOXB1 Transcription FactorsSurvival RateAgammaglobulinaemia Tyrosine KinaseBTK protein, humanProteomeSOX2 protein, humanSOXB1 Transcription Factors

Identifiers

PMID34645618
PMCPMC8548209
OpenAlexW3207226644

What OpenQuestion holds

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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.