Evidence map›Paper›PMID 35008316›Full record

ArticleCancers2021

BRG1 and NPM-ALK Are Co-Regulated in Anaplastic Large-Cell Lymphoma; BRG1 Is a Potential Therapeutic Target in ALCL.

Gavin D Garland, Stephen P Ducray, Leila Jahangiri, Perla Pucci, G A Amos Burke, Jack Monahan, Raymond Lai, Olaf Merkel, Ana-Iris Schiefer, Lukas Kenner and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. 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

12 authors at 9 institutions in 4 countries.

Gavin D GarlandDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge CB2 0QQ, UK.
Stephen P DucrayDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID 0000-0001-6407-1906
Leila JahangiriDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID 0000-0003-0235-8447
Perla PucciDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID 0000-0003-1264-3487
G A Amos BurkeDepartment of Paediatric Oncology, Cambridge University Hospital NHS Trust, Cambridge CB5 8PD, UK.
Jack MonahanThe European Bioinformatics Institute (EMBL EBI), Wellcome Genome Campus, Cambridge CB10 1SA, UK.
Raymond LaiDepartment of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB T6G 2R3, Canada.ORCID 0000-0002-6963-2407
Olaf MerkelDepartment of Pathology, Medical University Vienna, 1090 Vienna, Austria.
Ana-Iris SchieferDepartment of Pathology, Medical University Vienna, 1090 Vienna, Austria.ORCID 0000-0003-3555-8672
Lukas KennerDepartment of Pathology, Medical University Vienna, 1090 Vienna, Austria.ORCID 0000-0003-2184-1338
Andrew J BannisterThe Gurdon Institute, Cambridge CB2 1QN, UK.ORCID 0000-0002-6312-4436
Suzanne D TurnerDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID 0000-0002-8439-4507
University of Cambridge · GBMedical University of Vienna · ATBirmingham City University · GBCambridge University Hospitals NHS Foundation Trust · GBCentral European Institute of Technology · CZEuropean Bioinformatics Institute · GBThe Gurdon Institute · GBUniversity of Alberta · CAUniversity of Veterinary Medicine Vienna · AT

Funding

Cancer Research UK 17001Cancer Research UK C9685/A25117Marie Curie 675712
6 · The paper itself

Abstract

Anaplastic large-cell lymphoma (ALCL) is a T-cell malignancy driven in many cases by the product of a chromosomal translocation, nucleophosmin-anaplastic lymphoma kinase (NPM-ALK). NPM-ALK activates a plethora of pathways that drive the hallmarks of cancer, largely signalling pathways normally associated with cytokine and/or T-cell receptor-induced signalling. However, NPM-ALK is also located in the nucleus and its functions in this cellular compartment for the most part remain to be determined. We show that ALCL cell lines and primary patient tumours express the transcriptional activator BRG1 in a NPM-ALK-dependent manner. NPM-ALK regulates expression of BRG1 by post-translational mechanisms dependent on its kinase activity, protecting it from proteasomal degradation. Furthermore, we show that BRG1 drives a transcriptional programme associated with cell cycle progression. In turn, inhibition of BRG1 expression with specific shRNA decreases cell viability, suggesting that it may represent a key therapeutic target for the treatment of ALCL.

Indexed as

ALCLBrg1NPM-ALK

Identifiers

PMID35008316
PMCPMC8750310
OpenAlexW4200268997

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.