Evidence map›Paper›PMID 36575462›Full record

ReviewJournal of experimental & clinical cancer research : CR2022

Cellular senescence in cancer: clinical detection and prognostic implications.

Andreas Domen, Christophe Deben, Jasper Verswyvel, Tal Flieswasser, Hans Prenen, Marc Peeters, Filip Lardon, An Wouters

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
10.0field-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

53 citing papers in PubMed, 89 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Andreas DomenCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium. Andreas.Domen@uantwerpen.be.ORCID http://orcid.org/0000-0003-1398-3061
Christophe DebenCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium.
Jasper VerswyvelCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium.
Tal FlieswasserCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium.
Hans PrenenCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium.
Marc PeetersCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium.
Filip LardonCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium.
An WoutersCenter for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), University of Antwerp, 2610, Wilrijk (Antwerp), Belgium.
University of Antwerp · BE

Funding

Universiteit Antwerpen AntwerpUniversiteit Antwerpen Belgium (FFB180188 to AD)Universiteit Antwerpen University Research Fund (BOF) of the University of Antwerp
6 · The paper itself

Abstract

Cellular senescence is a state of stable cell-cycle arrest with secretory features in response to cellular stress. Historically, it has been considered as an endogenous evolutionary homeostatic mechanism to eliminate damaged cells, including damaged cells which are at risk of malignant transformation, thereby protecting against cancer. However, accumulation of senescent cells can cause long-term detrimental effects, mainly through the senescence-associated secretory phenotype, and paradoxically contribute to age-related diseases including cancer. Besides its role as tumor suppressor, cellular senescence is increasingly being recognized as an in vivo response in cancer patients to various anticancer therapies. Its role in cancer is ambiguous and even controversial, and senescence has recently been promoted as an emerging hallmark of cancer because of its hallmark-promoting capabilities. In addition, the prognostic implications of cellular senescence have been underappreciated due to the challenging detection and sparse in and ex vivo evidence of cellular senescence in cancer patients, which is only now catching up. In this review, we highlight the approaches and current challenges of in and ex vivo detection of cellular senescence in cancer patients, and we discuss the prognostic implications of cellular senescence based on in and ex vivo evidence in cancer patients.

Indexed as

Cellular SenescenceNeoplasmsCell Cycle CheckpointsCell Transformation, NeoplasticHumansPrognosisCancerDetectionOncogene-induced senescencePrognosisSASPSenescenceTherapy-induced senescence

Identifiers

PMID36575462
PMCPMC9793681
OpenAlexW4313250083

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.