Evidence map›Paper›PMID 29670296›Full record

ReviewBritish journal of cancer2018

Paracrine roles of cellular senescence in promoting tumourigenesis.

Jose Mario Gonzalez-Meljem, John Richard Apps, Helen Christina Fraser, Juan Pedro Martinez-Barbera

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 1 pooled it
9.2field-weighted citation impact, top 2% 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

111 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.

  1. Pooled it
  2. Review
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  12. Frontiers in immunology · 2026
    Article
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  14. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
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  17. Article
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51 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 2 countries.

Jose Mario Gonzalez-MeljemDevelopmental Biology and Cancer Research Programme, UCL Great Ormond Street Institute of Child Health, Guilford Street, London, WC1N 1EH, UK.
John Richard AppsDevelopmental Biology and Cancer Research Programme, UCL Great Ormond Street Institute of Child Health, Guilford Street, London, WC1N 1EH, UK.
Helen Christina FraserDevelopmental Biology and Cancer Research Programme, UCL Great Ormond Street Institute of Child Health, Guilford Street, London, WC1N 1EH, UK.
Juan Pedro Martinez-BarberaDevelopmental Biology and Cancer Research Programme, UCL Great Ormond Street Institute of Child Health, Guilford Street, London, WC1N 1EH, UK. j.martinez-barbera@ucl.ac.uk.
Great Ormond Street Hospital · GBUniversity College London · GB

Funding

Cancer Research UKMedical Research Council MR/M000125/1
6 · The paper itself

Abstract

Senescent cells activate genetic programmes that irreversibly inhibit cellular proliferation, but also endow these cells with distinctive metabolic and signalling phenotypes. Although senescence has historically been considered a protective mechanism against tumourigenesis, the activities of senescent cells are increasingly being associated with age-related diseases, including cancer. An important feature of senescent cells is the secretion of a vast array of pro-inflammatory cytokines, chemokines, and growth factors collectively known as the senescence-associated secretory phenotype (SASP). Recent research has shown that SASP paracrine signalling can mediate several pro-tumourigenic effects, such as enhancing malignant phenotypes and promoting tumour initiation. In this review, we summarise the paracrine activities of senescent cells and their role in tumourigenesis through direct effects on growth and proliferation of tumour cells, tumour angiogenesis, invasion and metastasis, cellular reprogramming and emergence of tumour-initiating cells, and tumour interactions with the local immune environment. The evidence described here suggests cellular senescence acts as a double-edged sword in cancer pathogenesis, which demands further attention in order to support the use of senolytic or SASP-modulating compounds for cancer treatment.

Indexed as

CarcinogenesisCell MovementCell ProliferationCellular ReprogrammingCellular SenescenceHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsParacrine Communication

Identifiers

PMID29670296
PMCPMC5959857
OpenAlexW2800736744

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.