Evidence map›Paper›PMID 32244751›Full record

ReviewMolecules (Basel, Switzerland)2020

Role of the Neutrophil in the Pathogenesis of Advanced Cancer and Impaired Responsiveness to Therapy.

Bernardo L Rapoport, Helen C Steel, Annette J Theron, Teresa Smit, Ronald Anderson

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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

5 authors at 2 institutions in 1 country.

Bernardo L RapoportDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.ORCID 0000-0001-7610-3653
Helen C SteelDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.ORCID 0000-0001-5899-4472
Annette J TheronDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.
Teresa SmitThe Medical Oncology Centre of Rosebank, Johannesburg 2196, South Africa.
Ronald AndersonDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.
University of Pretoria · ZAThe Medical Oncology Centre of Rosebank · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Notwithstanding the well-recognized involvement of chronic neutrophilic inflammation in the initiation phase of many types of epithelial cancers, a growing body of evidence has also implicated these cells in the pathogenesis of the later phases of cancer development, specifically progression and spread. In this setting, established tumors have a propensity to induce myelopoiesis and to recruit neutrophils to the tumor microenvironment (TME), where these cells undergo reprogramming and transitioning to myeloid-derived suppressor cells (MDSCs) with a pro-tumorigenic phenotype. In the TME, these MDSCs, via the production of a broad range of mediators, not only attenuate the anti-tumor activity of tumor-infiltrating lymphocytes, but also exclude these cells from the TME. Realization of the pro-tumorigenic activities of MDSCs of neutrophilic origin has resulted in the development of a range of adjunctive strategies targeting the recruitment of these cells and/or the harmful activities of their mediators of immunosuppression. Most of these are in the pre-clinical or very early clinical stages of evaluation. Notable exceptions, however, are several pharmacologic, allosteric inhibitors of neutrophil/MDSC CXCR1/2 receptors. These agents have entered late-stage clinical assessment as adjuncts to either chemotherapy or inhibitory immune checkpoint-targeted therapy in patients with various types of advanced malignancy. The current review updates the origins and identities of MDSCs of neutrophilic origin and their spectrum of immunosuppressive mediators, as well as current and pipeline MDSC-targeted strategies as potential adjuncts to cancer therapies. These sections are preceded by a consideration of the carcinogenic potential of neutrophils.

Indexed as

Disease SusceptibilityAnimalsCell Transformation, NeoplasticDisease ManagementHost-Pathogen InteractionsHumansImmunomodulationInflammationMyeloid-Derived Suppressor CellsNeoplasm MetastasisNeoplasmsNeoplasm StagingNeutrophilsOxidation-ReductionOxidative StressTreatment OutcomechemokinesCXC receptors 1 and 2granulocyte colony-stimulating factorimmune checkpoint inhibitorsimmunotherapymyeloid-derived suppressor cellsreactive oxygen speciesreparixinSX-682tumor-infiltrating lymphocytes

Identifiers

PMID32244751
PMCPMC7180559
OpenAlexW3014235009

What OpenQuestion 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 OpenQuestion graph.