Evidence map›Paper›PMID 41159617›Full record

ArticleSmall methods2025

A Reporter Platform to Study Therapy-Induced Senescence in Live Cancer Cells.

Jacinta van de Grint, Mengqi Huang, Ruben Sangers, Hanny Odijk, Thom Reuvers, Jose M Heredia-Genestar, Anja Raams, Tsung Wai Kan, Joris Pothof, Roland Kanaar and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Small methods, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Jacinta van de GrintDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Mengqi HuangDepartment of Pathology, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Ruben SangersDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Hanny OdijkDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Thom ReuversDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Jose M Heredia-GenestarDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Anja RaamsDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Tsung Wai KanDepartment of Pathology, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Joris PothofDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Roland KanaarDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.
Maayke M P KuijtenDepartment of Molecular Genetics, Oncode Institute, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, 3015 GD, the Netherlands.ORCID 0009-0001-2584-7473

Funding

Nederlandse Organisatie voor Wetenschappelijk Onderzoek 737.016.011Oncode Institute
6 · The paper itself

Abstract

Senescence is a durable state of cell cycle arrest that can be induced by various stressors, including DNA damage caused by chemotherapeutic agents or ionizing radiation. In the context of cancer, therapy-induced senescence (TIS) plays a dual role: while it effectively halts tumor cell proliferation, TIS also carries the risk of promoting tumor relapse through the senescence-associated secretory phenotype (SASP). Beyond its direct impact on tumor cells, cancer therapies leading to TIS often induce short- and long-term side effects that significantly affect the quality of life for patients. However, the lack of universal biomarkers for TIS hinders a comprehensive understanding of its characteristics and its role in cancer therapies. A lamin-based senescence reporter platform is developed to reliably detect and sort live senescent cancer cells. This versatile tool supports live-cell imaging, enabling real-time tracking of senescence induction and escape to investigate heterogeneity in treatment response. Additionally, it allows high-content screening and marker integration, for example incorporating IL6 as SASP marker. It is therefore a valuable tool for fundamental research addressing new questions in the field of TIS as well as for drug discovery, including the development of novel senolytics.

Indexed as

Cellular SenescenceNeoplasmsAntineoplastic AgentsCell Line, TumorGenes, ReporterHumansInterleukin-6Senescence-Associated Secretory PhenotypeAntineoplastic AgentsInterleukin-6DNA damagelaminslivemonitoringreportersenescence

Identifiers

PMID41159617
PMCPMC12716209

What OpenQuestion holds

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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.