Evidence map›Paper›PMID 25412306›Full record

ArticleCell death & disease2014

Characterization of novel markers of senescence and their prognostic potential in cancer.

M Althubiti, L Lezina, S Carrera, R Jukes-Jones, S M Giblett, A Antonov, N Barlev, G S Saldanha, C A Pritchard, K Cain and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
5.0field-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

149 citing papers in PubMed, 249 citations in OpenAlex.

  1. Identification of Hip BMD Loss and Fracture Risk Markers Through Population-Based Serum Proteomics.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017
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  10. Biomaterials science · 2025
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89 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 2 countries.

M Althubiti1] Department of Biochemistry, University of Leicester, Leicester, UK [2] Department of Biochemistry, Faculty of Medicine, Umm AL-Qura University, Mecca, Saudi Arabia.
L Lezina1] Department of Biochemistry, University of Leicester, Leicester, UK [2] Institute of Cytology RAS, Saint-Petersburg, Russia.
S CarreraDepartment of Biochemistry, University of Leicester, Leicester, UK.
R Jukes-JonesMRC Toxicology Unit, Leicester, UK.
S M GiblettDepartment of Biochemistry, University of Leicester, Leicester, UK.
A AntonovMRC Toxicology Unit, Leicester, UK.
N Barlev1] Department of Biochemistry, University of Leicester, Leicester, UK [2] Institute of Cytology RAS, Saint-Petersburg, Russia.
G S SaldanhaDepartment of Cancer Studies and Molecular Medicine, University of Leicester, Leicester, UK.
C A Pritchard1] Department of Biochemistry, University of Leicester, Leicester, UK [2] Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester, UK.
K Cain1] MRC Toxicology Unit, Leicester, UK [2] Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester, UK.
S MacipDepartment of Biochemistry, University of Leicester, Leicester, UK.
University of Leicester · GBMRC Toxicology Unit · GBInstitute of Cytology · RU

Funding

Cancer Research UK 13083Cancer Research UK 18370Medical Research Council
6 · The paper itself

Abstract

Cellular senescence is a terminal differentiation state that has been proposed to have a role in both tumour suppression and ageing. This view is supported by the fact that accumulation of senescent cells can be observed in response to oncogenic stress as well as a result of normal organismal ageing. Thus, identifying senescent cells in in vivo and in vitro has an important diagnostic and therapeutic potential. The molecular pathways involved in triggering and/or maintaining the senescent phenotype are not fully understood. As a consequence, the markers currently utilized to detect senescent cells are limited and lack specificity. In order to address this issue, we screened for plasma membrane-associated proteins that are preferentially expressed in senescent cells. We identified 107 proteins that could be potential markers of senescence and validated 10 of them (DEP1, NTAL, EBP50, STX4, VAMP3, ARMX3, B2MG, LANCL1, VPS26A and PLD3). We demonstrated that a combination of these proteins can be used to specifically recognize senescent cells in culture and in tissue samples and we developed a straightforward fluorescence-activated cell sorting-based detection approach using two of them (DEP1 and B2MG). Of note, we found that expression of several of these markers correlated with increased survival in different tumours, especially in breast cancer. Thus, our results could facilitate the study of senescence, define potential new effectors and modulators of this cellular mechanism and provide potential diagnostic and prognostic tools to be used clinically.

Indexed as

Agingbeta 2-MicroglobulinBiomarkers, TumorBreast NeoplasmsCell Line, TumorCellular SenescenceFemaleHumansMembrane ProteinsReceptor-Like Protein Tyrosine Phosphatases, Class 3Survival Analysisbeta 2-MicroglobulinBiomarkers, TumorMembrane ProteinsReceptor-Like Protein Tyrosine Phosphatases, Class 3

Identifiers

PMID25412306
PMCPMC4260747
OpenAlexW2050901509

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.