Evidence map›Paper›PMID 39217404›Full record

ReviewMolecular cancer2024

Cellular senescence and SASP in tumor progression and therapeutic opportunities.

Zening Dong, Yahan Luo, Zhangchen Yuan, Yu Tian, Tianqiang Jin, Feng Xu

Abstract readReview
In one paragraph

Review in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
174citing papers in PubMed, 2 pooled it
–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

174 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026
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  11. Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Interleukin-8 in health and disease.Molecular biomedicine · 2026
    Review
  17. Review
  18. Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
  19. Article
  20. Review

114 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

6 authors.

Zening Dong *Hepatobiliary and Splenic Surgery Ward, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, China.
Yahan Luo *Shanghai TCM-Integrated Hospital, Shanghai University of TCM, Shanghai, China.
Zhangchen YuanHepatobiliary and Splenic Surgery Ward, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, China.
Yu TianHepatobiliary and Splenic Surgery Ward, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, China.
Tianqiang JinHepatobiliary and Splenic Surgery Ward, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, China. jtq19950827@163.com.
Feng XuHepatobiliary and Splenic Surgery Ward, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, China. fxu@cmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence (CS), a permanent and irreversible arrest of the cell cycle and proliferation leading to the degeneration of cellular structure and function, has been implicated in various key physiological and pathological processes, particularly in cancer. Initially, CS was recognized as a barrier to tumorigenesis, serving as an intrinsic defense mechanism to protect cells from malignant transformation. However, increasing evidence suggests that senescent cells can promote tumor progression to overt malignancy, primarily through a set of factors known as senescence-associated secretory phenotypes (SASPs), including chemokines, growth factors, cytokines, and stromal metalloproteinases. These factors significantly reshape the tumor microenvironment (TME), enabling tumors to evade immune destruction. Interestingly, some studies have also suggested that SASPs may impede tumor development by enhancing immunosurveillance. These opposing roles highlight the complexity and heterogeneity of CS and SASPs in diverse cancers. Consequently, there has been growing interest in pharmacological interventions targeting CS or SASPs in cancer therapy, such as senolytics and senomorphics, to either promote the clearance of senescent cells or mitigate the harmful effects of SASPs. In this review, we will interpret the concept of CS, delve into the role of SASPs in reshaping the TME, and summarize recent advances in anti-tumor strategies targeting CS or SASPs.

Indexed as

Cellular SenescenceDisease ProgressionNeoplasmsSenescence-Associated Secretory PhenotypeTumor MicroenvironmentAnimalsHumansCellular senescenceSASPTherapyTumorTumor microenvironment

Identifiers

PMID39217404
PMCPMC11365203

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.