Evidence map›Paper›PMID 29345617›Full record

ArticleeLife2018

Loss of functional BAP1 augments sensitivity to TRAIL in cancer cells.

Krishna Kalyan Kolluri, Constantine Alifrangis, Neelam Kumar, Yuki Ishii, Stacey Price, Magali Michaut, Steven Williams, Syd Barthorpe, Howard Lightfoot, Sara Busacca and 21 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. An overview of BAP1 biological functions and current therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

31 authors at 7 institutions in 2 countries.

Krishna Kalyan Kolluri *Lungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0003-3537-0231
Constantine Alifrangis *Wellcome Trust Sanger Institute, Cambridge, United Kingdom.ORCID http://orcid.org/0000-0002-5876-6696
Neelam Kumar *Lungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0002-4346-2112
Yuki Ishii *Lungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.
Stacey PriceWellcome Trust Sanger Institute, Cambridge, United Kingdom.
Magali MichautThe Netherlands Cancer Institute, Amsterdam, Netherlands.ORCID http://orcid.org/0000-0003-2002-2277
Steven WilliamsWellcome Trust Sanger Institute, Cambridge, United Kingdom.ORCID http://orcid.org/0000-0002-9382-4337
Syd BarthorpeWellcome Trust Sanger Institute, Cambridge, United Kingdom.
Howard LightfootWellcome Trust Sanger Institute, Cambridge, United Kingdom.
Sara BusaccaCRUK Leicester Centre, Department of Cancer studies, University of Leicester, Leicester, United Kingdom.
Annabel SharkeyCRUK Leicester Centre, Department of Cancer studies, University of Leicester, Leicester, United Kingdom.
Zhenqiang YuanLungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.
Elizabeth K SageLungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0002-9009-421X
Sabarinath VallathLungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.
John Le QuesneCRUK Leicester Centre, Department of Cancer studies, University of Leicester, Leicester, United Kingdom.
David A TiceOncology Research, MedImmune, Inc., Gaithersburg, United States.
Doraid AlrifaiLungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.
Sylvia von KarstedtCentre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, United Kingdom.
Antonella MontinaroCentre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, United Kingdom.
Naomi GuppyUCL Advanced Diagnostics, University College London, London, United Kingdom.
David A WallerDepartment of Thoracic Surgery, Glenfield Hospital, University Hospitals of Leicester, Leicester, United Kingdom.
Apostolos NakasDepartment of Thoracic Surgery, Glenfield Hospital, University Hospitals of Leicester, Leicester, United Kingdom.
Robert GoodUCL School of Pharmacy, University College London, London, United Kingdom.
Alan HolmesUCL School of Pharmacy, University College London, London, United Kingdom.
Henning WalczakCentre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, London, United Kingdom.
Dean A FennellCRUK Leicester Centre, Department of Cancer studies, University of Leicester, Leicester, United Kingdom.
Mathew GarnettWellcome Trust Sanger Institute, Cambridge, United Kingdom.
Francesco IorioEuropean Molecular Biology Laboratory, European Bioinformatics Institute, Cambridge, United Kingdom.
Lodewyk WesselsThe Netherlands Cancer Institute, Amsterdam, Netherlands.
Ultan McDermottWellcome Trust Sanger Institute, Cambridge, United Kingdom.
Samuel M JanesLungs for Living Research Centre, UCL Respiratory, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0002-6634-5939
University College London · GBWellcome Sanger Institute · GBUniversity of Leicester · GBCRUK Lung Cancer Centre of Excellence · GBGlenfield Hospital · GBThe Netherlands Cancer Institute · NLEuropean Bioinformatics Institute · GB

Funding

Cancer Research UK A17341Medical Research Council MC_UP_1203/1Medical Research Council MR/M015831/1Wellcome TrustWellcome Trust 106555/Z/14/ZWellcome Trust WT107963AIA
6 · The paper itself

Abstract

Malignant mesothelioma (MM) is poorly responsive to systemic cytotoxic chemotherapy and invariably fatal. Here we describe a screen of 94 drugs in 15 exome-sequenced MM lines and the discovery of a subset defined by loss of function of the nuclear deubiquitinase BRCA associated protein-1 (BAP1) that demonstrate heightened sensitivity to TRAIL (tumour necrosis factor-related apoptosis-inducing ligand). This association is observed across human early passage MM cultures, mouse xenografts and human tumour explants. We demonstrate that BAP1 deubiquitinase activity and its association with ASXL1 to form the Polycomb repressive deubiquitinase complex (PR-DUB) impacts TRAIL sensitivity implicating transcriptional modulation as an underlying mechanism. Death receptor agonists are well-tolerated anti-cancer agents demonstrating limited therapeutic benefit in trials without a targeting biomarker. We identify

Indexed as

AnimalsCell Line, TumorHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantMiceRepressor ProteinsTNF-Related Apoptosis-Inducing LigandTumor Suppressor ProteinsUbiquitin ThiolesteraseASXL1 protein, humanBAP1 protein, humanRepressor ProteinsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1cancer biologyhumanhuman biologymedicinemesotheliomamousePR-DUBTRAIL

Identifiers

PMID29345617
PMCPMC5773178
OpenAlexW2783370725

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.