Evidence map›Paper›PMID 39849183›Full record

ReviewClinical and experimental medicine2025

Cellular senescence in the tumor with a bone niche microenvironment: friend or foe?

Sajad Alavimanesh, Negar Nayerain Jazi, Maedeh Choubani, Farzane Saeidi, Hamed Afkhami, Aref Yarahmadi, Hossein Ronaghi, Pouria Khani, Mohammad Hossein Modarressi

Abstract readReview
In one paragraph

Review in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
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

9 authors.

Sajad AlavimaneshStudent Research Committee, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Negar Nayerain JaziStudent Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
Maedeh ChoubaniSchool of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Farzane SaeidiDepartment of Medical Genetics, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Hamed AfkhamiCellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran.
Aref YarahmadiDepartment of Biology, Khorramabad Branch, Islamic Azad University, Khorramabad, Iran.
Hossein RonaghiDepartment of Orthopedic, Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Pouria KhaniDepartment of Medical Genetics, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran. Pouriakhani70@gmail.com.
Mohammad Hossein ModarressiDepartment of Medical Genetics, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran. modaresi@tums.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is understood to be a biological process that is defined as irreversible growth arrest and was originally recognized as a tumor-suppressive mechanism that prevents further propagation of damaged cells. More recently, cellular senescence has been shown to have a dual role in prevention and tumor promotion. Senescent cells carry a senescence-associated secretory phenotype (SASP), which is altered by secretory factors including pro-inflammatory cytokines, chemokines, and other proteases, leading to the alteration of the tissue microenvironment. Though senescence would eventually halt the growth of cancerous potential cells, SASP contributes to the tumor environment by promoting inflammation, matrix remodeling, and tumor cell invasion. The paradox of tumor prevention/promotion is particularly relevant to the bone niche tumor microenvironment, where longer-lasting, chronic inflammation promotes tumor formation. Insights into a mechanistic understanding of cellular senescence and SASP provide the basis for targeted therapies, such as senolytics, which aim to eliminate senescent cells, or SASP inhibitors, which would eliminate the tumor-promoting effects of senescence. These therapeutic interventions offer significant clinical implications for treating cancer and healthy aging.

Indexed as

Bone and BonesCellular SenescenceNeoplasmsSenescence-Associated Secretory PhenotypeTumor MicroenvironmentAnimalsHumansBone nicheCellular senescenceSenescence-associated secretory phenotype (SASP)Tumor microenvironment

Identifiers

PMID39849183
PMCPMC11759293

What OpenQuestion holds

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Registered trials

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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.