Evidence map›Paper›PMID 31821533›Full record

ReviewImmunology2020

Blocking inflammation to improve immunotherapy of advanced cancer.

Antonio Macciò, Clelia Madeddu

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% of its field
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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Molecular Basis and Advances in Targeted Immunotherapy for Cancer.International journal of molecular sciences · 2023
    Article
  16. Article
  17. Article
  18. Article
  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

2 authors at 2 institutions in 1 country.

Antonio MacciòDepartment of Gynecologic Oncology, Azienda Ospedaliera Brotzu, Cagliari, Italy.ORCID 0000-0003-0577-7217
Clelia MadedduDepartment of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.ORCID 0000-0001-8940-6987
Azienda Ospedaliera G. Brotzu · ITUniversity of Cagliari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability to induce functional reprogramming of regulatory T (Treg) cells in the tumor microenvironment is an extremely important therapeutic opportunity. However, when discussing such an approach, the opposing effect that the activation of the Treg cell compartments may have in inducing the immune inflammatory response and its link with the efficacy of immunotherapy should be considered. In fact, Treg reprogramming has a dual effect: immediate, with mechanisms that activate immunosurveillance, and late, mediated by the macrophage activation that yields an inflammatory status that is deleterious for the antineoplastic efficiency of the immune system response. Persistence of the inflammatory response is associated with specific changes of oxidative and glycolytic metabolic pathways that interfere with conventional T-cell activation and function and may be one of the reasons for the failure of immunotherapy in advanced cancer patients. Therefore, in addition to modulating Treg cell action, the combined use of drugs able to block chronic inflammation mediated mainly by macrophages, to counteract the oxidative stress, and to positively regulate the metabolic derangements, could improve the effectiveness of modern immunotherapy. In conclusion, reprogramming of Treg cells may be an appropriate strategy for treating early stages of neoplastic diseases, whereas other immunosuppressive mechanisms should be the target of a combined immunotherapy approach in more advanced phases of cancer.

Indexed as

Anti-Inflammatory AgentsAntineoplastic AgentsCellular ReprogrammingDisease ProgressionGlycolysisHumansImmunologic FactorsImmunologic SurveillanceImmunotherapyInflammationLymphocyte ActivationMacrophage ActivationMacrophagesNeoplasmsOxidative PhosphorylationT-Lymphocytes, RegulatoryAnti-Inflammatory AgentsAntineoplastic AgentsImmunologic Factorsimmunotherapyinflammationmacrophagesregulatory T cellstumor immunology

Identifiers

PMID31821533
PMCPMC7078000
OpenAlexW2996421579

What OpenQuestion holds

Textmetadata
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.