Evidence map›Paper›PMID 31130612›Full record

ReviewBiomolecules2019

Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update.

Marco Casciaro, Roberta Cardia, Eleonora Di Salvo, Giovanni Tuccari, Antonio Ieni, Sebastiano Gangemi

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases.International journal of molecular sciences · 2019
    Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. IL-33 genetics and epigenetics in immune-related diseases.Clinical and molecular allergy : CMA · 2021
    Article
  10. Article
  11. Review
  12. Dual role of interleukin-33 in tumors.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    Article
  13. Article
  14. Article
  15. The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox.International journal of molecular sciences · 2019
    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

6 authors at 2 institutions in 1 country.

Marco CasciaroSchool and Unit of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University of Messina, 98123 Messina, Italy. mcasciaro@unime.it.
Roberta CardiaDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Section of Pathology, University of Messina, 98123 Messina, Italy. robertacardia87@hotmail.com.
Eleonora Di SalvoNational Research Council of Italy (CNR), Institute of Biological Resources and Marine Biotechnologies (IRBIM), 98122 Messina, Italy. e.disalvo@isasi.cnr.it.
Giovanni TuccariDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Section of Pathology, University of Messina, 98123 Messina, Italy. tuccari@unime.it.
Antonio IeniDepartment of Human Pathology in Adult and Developmental Age "Gaetano Barresi", Section of Pathology, University of Messina, 98123 Messina, Italy. aieni@unime.it.ORCID 0000-0003-2878-3572
Sebastiano GangemiSchool and Unit of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University of Messina, 98123 Messina, Italy. gangemis@unime.it.
University of Messina · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung carcinogenesis is a multistep process involving genetic mutations and epigenetic changes, with the acquisition of a malignant phenotype characterized by apoptosis resistance, unregulated proliferation and differentiation, invasion, and metastatic abilities. However, neoplastic development and progression seem to be aided by non-neoplastic cells; the molecules they produced can either promote the immune response or, alternatively, support tumor pathogenesis. Consequently, the relative contribution of tumor-associated inflammatory pathways to cancer development has become crucial information. Interleukin-33 (IL-33) is an IL-1-like alarmin, and it is a ligand for the suppressor of tumorigenicity 2 (ST2) receptor. IL-33 functions as a dual role cytokine with the ability to induce T-helper-type 2 (Th2) immune cells and translocate into the nucleus, suppressing gene transcription. Although its function in immunity- and immune-related disorders is well known, its role in tumorigenesis is still debated. The IL-33/ST2 axis is emerging as a powerful modulator of the tumor microenvironment (TME) by recruiting immune cells, able to modify the TME, supporting malignant proliferation or improving antitumor immunity. In the present review, we discuss IL-33's potential role in lung carcinogenesis and its possible application as a therapeutic target.

Indexed as

AnimalsCarcinogenesisCarcinoma, Non-Small-Cell LungHumansInterleukin-33Lung NeoplasmsReceptors, InterleukinInterleukin-33Receptors, InterleukincancerIL-33immune systemimmunotherapylung

Identifiers

PMID31130612
PMCPMC6572046
OpenAlexW2944837039

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.