Evidence mapPaperPMID 40420174Full record

ReviewJournal of translational medicine2025

Targeting inflammation in cancer therapy: from mechanistic insights to emerging therapeutic approaches.

Saad Bakrim, Meriem El Fessikh, Hamza Elhrech, Nasreddine El Omari, Mohammed Amanullah, Long Chiau Ming, Said Moshawih, Abdelhakim Bouyahya

Abstract readReview
In one paragraph

Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

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

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

8 authors.

Saad BakrimGeo-Bio-Environment Engineering and Innovation Laboratory, Molecular Engineering, Biotechnology and Innovation Team, Polydisciplinary Faculty of Taroudant, Ibn Zohr University, Agadir, 80000, Morocco.
Meriem El FessikhLaboratory of Human Pathologies Biology, Faculty of Sciences, Mohammed V University in Rabat, Rabat, Morocco.
Hamza ElhrechLaboratory of Human Pathologies Biology, Faculty of Sciences, Mohammed V University in Rabat, Rabat, Morocco.
Nasreddine El OmariHigh Institute of Nursing Professions and Health Techniques of Tetouan, Tetouan, Morocco.
Mohammed AmanullahDepartment of clinical Biochemistry, College of Medicine, King Khalid University, Abha, Kingdom of Saudi Arabia.
Long Chiau MingDatta Meghe College of Pharmacy, Datta Meghe Institute of Higher Education and Research (deemed to be University), Sawangi (M), Wardha, India.
Said MoshawihDepartment of Pharmaceutical Sciences, Faculty of Pharmacy, Al-Ahliyya Amman University, Amman, Jordan.
Abdelhakim BouyahyaLaboratory of Human Pathologies Biology, Faculty of Sciences, Mohammed V University in Rabat, Rabat, Morocco. a.bouyahya@um5r.ac.ma.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a complex and finely tuned component of the host defense mechanism, responding sensitively to a range of physical, chemical, and biological stressors. Current research is advancing our grasp of both cellular and molecular mechanisms that initiate and regulate interactions within inflammatory pathways. Substantial evidence now indicates a profound link between inflammation, innate immunity, and cancer. Dysregulation of inflammatory pathways is known to be a pivotal factor in the induction, growth, and metastasis of tumors through multiple mechanistic pathways. Basically, the tumor microenvironment (TME), characterized by dynamic interplay between cancerous cells and surrounding inflammatory and stromal cells, plays a central role in these processes. Increasingly, controlled acute inflammation is being explored as a promising therapeutic tool in certain types of cancer. However, inflammatory cells in the TME exhibit remarkable plasticity, with shifting phenotypic and functional roles that facilitate cancer cell survival, proliferation, and migration, especially under chronic inflammatory conditions. Additionally, signaling molecules associated with the innate immune system, like chemokines, are co-opted by malignant cells to support invasion, migration, and metastasis. These findings underscore the need for deeper insights into the mechanisms connecting inflammation to cancer pathology, which could pave the way for innovative diagnostic approaches and targeted anti-inflammatory therapies to counter tumor development. The current review underlines the critical involvement of inflammation in cancer development, examining the connection between the immune system, key inflammatory mediators, biomarkers, and their associated pathways in cancer. We also discuss the impact of inflammation-targeted therapies on anticancer signaling pathways. Furthermore, we review major anti-inflammatory drugs with potential applications in oncology, assessing how inflammation is modulated in cancer management. Lastly, we outline an overview of ongoing discoveries in the field, highlighting both the challenges and the therapeutic promise of targeting inflammation in cancer therapy.

Indexed as

InflammationMolecular Targeted TherapyNeoplasmsAnimalsHumansSignal TransductionTumor MicroenvironmentAnti-inflammatory drugsCancerInflammationInflammation-targeted therapyInflammatory mediatorsInnate immunitySignaling pathways

Identifiers

PMID40420174
PMCPMC12107871

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.