Evidence map›Paper›PMID 30742053›Full record

ArticleScientific reports2019

IL1RL1 is dynamically expressed on Cbfb-MYH11

Yiqian Wang, Lisa Richter, Michelle Becker, Catalina Amador, R Katherine Hyde

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
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  8. Article
  9. The role of IL-33/ST2 signaling in the tumor microenvironment and Treg immunotherapy.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox.International journal of molecular sciences · 2019
    Review
  14. OncoTargets and therapy · 2019
    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 1 institution in 1 country.

Yiqian WangDepartment of Biochemistry and Molecular Biology, and Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, United States.
Lisa RichterDepartment of Biochemistry and Molecular Biology, and Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, United States.
Michelle BeckerDepartment of Biochemistry and Molecular Biology, and Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, United States.
Catalina AmadorDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, United States.
R Katherine HydeDepartment of Biochemistry and Molecular Biology, and Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, United States. kate.hyde@unmc.edu.
University of Nebraska Medical Center · US

Funding

Analysis of Initiating Events in Inv(16) Associated Acute Myeloid LeukemiaR00CA148963 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HYDE, RICIA KATHERINE · 2013 to 2015
$725k
NCI NIH HHS R00 CA148963
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is often characterized by the presence of specific, recurrent chromosomal abnormalities. One of the most common aberrations, inversion of chromosome 16 [inv(16)], generates the fusion oncogene CBFB-MYH11. Previously, we used a mouse knock-in model to show that Cbfb-MYH11 induces changes in gene expression and results in the accumulation of abnormal myeloid cells, a subset of which are enriched for leukemia stem cell (LSC) activity. One gene upregulated by Cbfb-MYH11 encodes the cytokine receptor IL1RL1 (ST2). IL1RL1 and its ligand IL-33 are known regulators of mature myeloid cells, but their roles in AML are not known. Here, we use Cbfb-MYH11 knock-in mice to show that IL1RL1 is expressed by cell populations with high LSC activity, and that the cell surface expression of IL1RL1 is dynamic, implying that the expression of IL1RL1 is not restricted to a specific stage of differentiation. We also show that treatment with IL-33 increased serial replating ability and expression of pro-survival proteins in vitro. Finally, we show that IL1RL1

Indexed as

Gene Expression Regulation, LeukemicAntineoplastic AgentsCell Line, TumorCell ProliferationCell SurvivalCytokine Receptor Common beta SubunitHumansInterleukin-1 Receptor-Like 1 ProteinLeukemia, Myeloid, AcuteNeoplastic Stem CellsOncogene Proteins, FusionSignal TransductionAntineoplastic AgentsCBFbeta-MYH11 fusion proteinCSF2RB protein, humanCytokine Receptor Common beta SubunitIL1RL1 protein, humanInterleukin-1 Receptor-Like 1 ProteinOncogene Proteins, Fusion

Identifiers

PMID30742053
PMCPMC6370767
OpenAlexW2940449217

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.