Evidence map›Paper›PMID 31652497›Full record

ReviewInternational journal of molecular sciences2019

The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox.

Alessandro Allegra, Vanessa Innao, Gennaro Tartarisco, Giovanni Pioggia, Marco Casciaro, Caterina Musolino, Sebastiano Gangemi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Bone Marrow-Derived C-KitApplied biochemistry and biotechnology · 2024
    Article
  6. Article
  7. Review
  8. The role of IL-33/ST2 signaling in the tumor microenvironment and Treg immunotherapy.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. 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

7 authors at 2 institutions in 1 country.

Alessandro AllegraDivision of Hematology, Department of Human Pathology in Adulthood and Childhood, University of Messina, 98125 Messina, Italy. aallegra@unime.it.ORCID 0000-0001-6156-8239
Vanessa InnaoDivision of Hematology, Department of Human Pathology in Adulthood and Childhood, University of Messina, 98125 Messina, Italy. vinnao@unime.it.
Gennaro TartariscoNational Research Council of Italy (CNR)-Institute for Biomedical Research and Innovation (IRIB), 98164 Messina, Italy. gennaro.tartarisco@cnr.it.
Giovanni PioggiaNational Research Council of Italy (CNR)-Institute for Biomedical Research and Innovation (IRIB), 98164 Messina, Italy. giovanni.pioggia@cnr.it.
Marco CasciaroSchool and Division of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University Hospital "G. Martino", Via Consolare Valeria SNC, 98125 Messina, Italy. mcasciaro@unime.it.
Caterina MusolinoDivision of Hematology, Department of Human Pathology in Adulthood and Childhood, University of Messina, 98125 Messina, Italy. cmusolino@unime.it.
Sebastiano GangemiSchool and Division of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University Hospital "G. Martino", Via Consolare Valeria SNC, 98125 Messina, Italy. gangemis@unime.it.
University of Messina · ITInstitute for Biomedical Research and Innovation · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-33 is a chromatin-related nuclear interleukin that is a component of IL-1 family. IL-33 production augments the course of inflammation after cell damage or death. It is discharged into the extracellular space. IL-33 is regarded as an "alarmin" able to stimulate several effectors of the immune system, regulating numerous immune responses comprising cancer immune reactions. IL-33 has been demonstrated to influence tumorigenesis. However, as far as this cytokine is concerned, we are faced with what has sometimes been defined as the IL-33 paradox. Several studies have demonstrated a relevant role of IL-33 to numerous malignancies, where it may have pro- and-less frequently-antitumorigenic actions. In the field of hematological malignancies, the role of IL-33 seems even more complex. Although we can affirm the existence of a negative role of IL-33 in Chronic myelogenos leukemia (CML) and in lymphoproliferative diseases and a positive role in pathologies such as Acute myeloid leukemia (AML), the action of IL-33 seems to be multiple and sometimes contradictory within the same pathology. In the future, we will have to learn to govern the negative aspects of activating the IL-33/ST2 axis and exploit the positive ones.

Indexed as

AnimalsHematologic NeoplasmsHumansInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Signal TransductionInterleukin-1 Receptor-Like 1 ProteinInterleukin-33alarminhematologic malignanciesimmune responseinterleukin 33tumorigenesis

Identifiers

PMID31652497
PMCPMC6834139
OpenAlexW2981045429

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.