Evidence map›Paper›PMID 39120312›Full record

ReviewCells2024

Therapy-Induced Cellular Senescence: Potentiating Tumor Elimination or Driving Cancer Resistance and Recurrence?

Yue Liu, Isabelle Lomeli, Stephen J Kron

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

  1. Review
  2. Mechanisms and therapeutic potential of therapy-induced cellular senescence in radiotherapy- and chemotherapy-related alimentary tract mucositis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
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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

3 authors.

Yue LiuLudwig Center for Metastasis Research and Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA.
Isabelle LomeliLudwig Center for Metastasis Research and Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA.
Stephen J KronLudwig Center for Metastasis Research and Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA.ORCID 0000-0003-1518-2436

Funding

Systemic delivery of siRNA by Nanosac for checkpoint blockade immunotherapy of head and neck squamous cell cancerR01CA258737 · NCI · PURDUE UNIVERSITY · PI KRON, STEPHEN J., YEO, YOON · 2021 to 2024
$2.3M
Bioinspired chemical probe approach targeting telomerase reverse transcriptaseR01CA254047 · NCI · NORTHWESTERN UNIVERSITY · PI KRON, STEPHEN J., SCHEIDT, KARL A · 2020 to 2024
$1.9M
PAIRS: Validating telomerase reverse transcriptase (TERT) as an intrinsic vulnerability toward sensitizing cancer to radiationR01CA282781 · NCI · UNIVERSITY OF CHICAGO · PI Stephen J. Kron, Karl A Scheidt · 2023 to 2026
$1.9M
Lipid signaling in cellular senescence and tissue agingR01AG069865 · NIA · UNIVERSITY OF CHICAGO · PI KRON, STEPHEN J. · 2020 to 2024
$1.8M
Targets of Reactive Lipid Species regulating DNA damage response and cell senescenceR01CA217182 · NCI · UNIVERSITY OF CHICAGO · PI KRON, STEPHEN J. · 2017 to 2021
$1.7M
CDMRP PRCRP Impact Award CA190982NCI NIH HHS R01 CA217182NCI NIH HHS R01 CA254047NCI NIH HHS R01 CA258737NCI NIH HHS R01 CA282781NIA NIH HHS R01 AG069865NIH HHS AG069865NIH HHS CA217182NIH HHS CA254047NIH HHS CA282781
6 · The paper itself

Abstract

Cellular senescence has been increasingly recognized as a hallmark of cancer, reflecting its association with aging and inflammation, its role as a response to deregulated proliferation and oncogenic stress, and its induction by cancer therapies. While therapy-induced senescence (TIS) has been linked to resistance, recurrence, metastasis, and normal tissue toxicity, TIS also has the potential to enhance therapy response and stimulate anti-tumor immunity. In this review, we examine the Jekyll and Hyde nature of senescent cells (SnCs), focusing on how their persistence while expressing the senescence-associated secretory phenotype (SASP) modulates the tumor microenvironment through autocrine and paracrine mechanisms. Through the SASP, SnCs can mediate both resistance and response to cancer therapies. To fulfill the unmet potential of cancer immunotherapy, we consider how SnCs may influence tumor inflammation and serve as an antigen source to potentiate anti-tumor immune response. This new perspective suggests treatment approaches based on TIS to enhance immune checkpoint blockade. Finally, we describe strategies for mitigating the detrimental effects of senescence, such as modulating the SASP or targeting SnC persistence, which may enhance the overall benefits of cancer treatment.

Indexed as

Cellular SenescenceDrug Resistance, NeoplasmNeoplasmsAnimalsHumansImmunotherapyNeoplasm Recurrence, LocalSenescence-Associated Secretory PhenotypeTumor Microenvironmentcancer therapyimmune surveillanceimmunosuppressionSASP (senescence-associated secretory phenotype)senescencesenolyticstherapy resistancetumor microenvironment

Identifiers

PMID39120312
PMCPMC11312217

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.