Evidence map›Paper›PMID 40781676›Full record

ReviewMolecular cancer2025

Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.

Tiejun Feng, Fuda Xie, Leo M Y Lee, Zhiqiang Lin, Yifan Tu, Yang Lyu, Peiyao Yu, Jialin Wu, Bonan Chen, Ge Zhang and 3 more

Abstract readReview
In one paragraph

Review in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Dysregulated mScience advances · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. The Role of Selected Bacteria in Breast Cancer Initiation and Development.International journal of molecular sciences · 2026
    Review
  13. Article
  14. IL-15 Plus Thymosin α1 Reduces Senescent Hepatic CD8Journal of gastroenterology and hepatology · 2026
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

13 authors.

Tiejun FengDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Fuda XieDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Leo M Y LeeDepartment of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hong Kong, China.
Zhiqiang LinNational Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, China.
Yifan TuDepartment of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Hong Kong, China.
Yang LyuDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Peiyao YuDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Jialin WuDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Bonan ChenDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Ge ZhangLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases (TMBJ), School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Gary M K TseDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Ka Fai ToDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Wei KangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China. weikang@cuhk.edu.hk.

Funding

CUHK direct research grant 2024.066National Natural Science Foundation of China 82272990NSFC-RGC Joint Research Scheme N_CUHK448/23
6 · The paper itself

Abstract

Cellular senescence is a double-edged sword in cancer biology, functioning as both a tumor-suppressive mechanism and a driver of malignancy. Initially, senescence acts as a protective barrier by arresting the proliferation of damaged or oncogene-expressing cells via pathways such as oncogene-induced senescence and the DNA damage response. However, persistent senescence-associated secretory phenotype and metabolic reprogramming in senescent cells create a pro-inflammatory, immunosuppressive tumor microenvironment, fueling cancer progression, therapy resistance, and metastasis. This comprehensive review systematically examines the molecular mechanisms of senescence across diverse cancers, spanning digestive, reproductive, urinary, respiratory, nervous, hematologic, endocrine, and integumentary systems, and elucidates its context-dependent roles in tumor suppression and promotion. We highlight groundbreaking therapeutic innovations, including precision senolytics, senomorphics, and combinatorial strategies integrating immunotherapy, metabolic interventions, and epigenetic modulators. The review also addresses microenvironment remodeling and cutting-edge technologies for dissecting senescence heterogeneity, epigenetic clocks for biological age prediction, and microbiome engineering to modulate senescence. Despite their promise, challenges such as off-target effects, biomarker limitations, and cellular heterogeneity underscore the need for precision medicine approaches. Finally, we propose future directions to harness senescence as a dynamic therapeutic target, offering transformative potential for cancer treatment.

Indexed as

Cellular SenescenceNeoplasmsPrecision MedicineAnimalsHumansTumor MicroenvironmentCancerSenescenceTherapeutic innovation

Identifiers

PMID40781676
PMCPMC12333312

What Socratic 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 Socratic graph.