Evidence map›Paper›PMID 29367434›Full record

ArticleMolecular & cellular proteomics : MCP2018

Proteomics Profiling of CLL Versus Healthy B-cells Identifies Putative Therapeutic Targets and a Subtype-independent Signature of Spliceosome Dysregulation.

Harvey E Johnston, Matthew J Carter, Marta Larrayoz, James Clarke, Spiro D Garbis, David Oscier, Jonathan C Strefford, Andrew J Steele, Renata Walewska, Mark S Cragg

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  8. Systematic Multiomic Analysis ofInternational journal of molecular sciences · 2023
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  17. Kinobead Profiling Reveals Reprogramming of BCR Signaling in Response to Therapy within Primary CLL Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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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

10 authors at 3 institutions in 1 country.

Harvey E JohnstonFrom the ‡Antibody and Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, General Hospital, University of Southampton, Southampton, UK.
Matthew J CarterFrom the ‡Antibody and Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, General Hospital, University of Southampton, Southampton, UK.
Marta Larrayoz¶Cancer Genomics, Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton, UK.
James Clarke‖Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton, UK.
Spiro D Garbis§Centre for Proteomic Research, Institute for Life Sciences, University of Southampton, Highfield Campus, Southampton, UK.
David Oscier‡‡Department of Molecular Pathology, Royal Bournemouth Hospital, Bournemouth, UK.
Jonathan C Strefford¶Cancer Genomics, Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton, UK.
Andrew J Steele§§Leukemia and Lymphoma Molecular Mechanisms and Therapy Group, Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton, UK.
Renata Walewska¶¶Department of Haematology, Royal Bournemouth Hospital, Bournemouth, UK.
Mark S CraggFrom the ‡Antibody and Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, General Hospital, University of Southampton, Southampton, UK; msc@soton.ac.uk.
University of Southampton · GBRoyal Bournemouth Hospital · GBSouthampton General Hospital · GB

Funding

Cancer Research UK 23669Cancer Research UK C24563/A15581Cancer Research UK C34999/A18087Medical Research Council
6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) is a heterogeneous B-cell cancer exhibiting a wide spectrum of disease courses and treatment responses. Molecular characterization of RNA and DNA from CLL cases has led to the identification of important driver mutations and disease subtypes, but the precise mechanisms of disease progression remain elusive. To further our understanding of CLL biology we performed isobaric labeling and mass spectrometry proteomics on 14 CLL samples, comparing them with B-cells from healthy donors (HDB). Of 8694 identified proteins, ∼6000 were relatively quantitated between all samples (q<0.01). A clear CLL signature, independent of subtype, of 544 significantly overexpressed proteins relative to HDB was identified, highlighting established hallmarks of CLL (

Indexed as

B-LymphocytesHumansLeukemia, Lymphocytic, Chronic, B-CellNeoplasm ProteinsProteomicsSpliceosomesNeoplasm Proteins

Identifiers

PMID29367434
PMCPMC5880099
OpenAlexW2785372204

What OpenQuestion holds

Textmetadata
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.