Evidence map›Paper›PMID 30737084›Full record

ReviewEBioMedicine2019

Senolytics and senostatics as adjuvant tumour therapy.

Susan Short, Edward Fielder, Satomi Miwa, Thomas von Zglinicki

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 1 pooled it
15.4field-weighted citation impact, top 1% 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

131 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
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71 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

4 authors at 2 institutions in 1 country.

Susan ShortLeeds Institute of Cancer and Pathology, Wellcome Trust Brenner Building, St James's University Hospital, Beckett St, Leeds LS9 7TF, UK.
Edward FielderNewcastle University Institute for Ageing, Institute for Cell and Molecular Biology, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.
Satomi MiwaNewcastle University Institute for Ageing, Institute for Cell and Molecular Biology, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.
Thomas von ZglinickiNewcastle University Institute for Ageing, Institute for Cell and Molecular Biology, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne NE4 5PL, UK. Electronic address: t.vonzglinicki@ncl.ac.uk.
Newcastle Hospitals - Campus for Ageing and Vitality · GBSt James's University Hospital · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F010966/1Biotechnology and Biological Sciences Research Council BB/I020748/1Biotechnology and Biological Sciences Research Council BB/S006710/1Cancer Research UK 24009Medical Research Council MR/P020941/1
6 · The paper itself

Abstract

Cell senescence is a driver of ageing, frailty, age-associated disease and functional decline. In oncology, tumour cell senescence may contribute to the effect of adjuvant therapies, as it blocks tumour growth. However, this is frequently incomplete, and tumour cells that recover from senescence may gain a more stem-like state with increased proliferative potential. This might be exaggerated by the induction of senescence in the surrounding niche cells. Finally, senescence will spread through bystander effects, possibly overwhelming the capacity of the immune system to ablate senescent cells. This induces a persistent system-wide senescent cell accumulation, which we hypothesize is the cause for the premature frailty, multi-morbidity and increased mortality in cancer survivors. Senolytics, drugs that selectively kill senescent cells, have been developed recently and have been proposed as second-line adjuvant tumour therapy. Similarly, by blocking accelerated senescence following therapy, senolytics might prevent and potentially even revert premature frailty in cancer survivors. Adjuvant senostatic interventions, which suppress senescence-associated bystander signalling, might also have therapeutic potential. This becomes pertinent because treatments that are senostatic in vitro (e.g. dietary restriction mimetics) persistently reduce numbers of senescent cells in vivo, i.e. act as net senolytics in immunocompetent hosts.

Indexed as

AnimalsAntineoplastic AgentsBystander EffectCellular SenescenceDNA DamageHumansNeoplasmsRadiation, IonizingAntineoplastic AgentsCancerGliomaSenolyticsSenostaticsSurvivorTherapy

Identifiers

PMID30737084
PMCPMC6441870
OpenAlexW2915058673

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.