Evidence map›Paper›PMID 32793603›Full record

ArticleFrontiers in cell and developmental biology2020

Acute Myeloid Leukemia Chemo-Resistance Is Mediated by E-selectin Receptor CD162 in Bone Marrow Niches.

Johanna Erbani, Joshua Tay, Valerie Barbier, Jean-Pierre Levesque, Ingrid G Winkler

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  9. PSGL-1 decorated with sialyl LewisScientific reports · 2024
    Article
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  14. The biology of E-selectin ligands in leukemogenesis.Advances in cancer research · 2023
    Review
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  17. Article
  18. IntegratedCells · 2021
    Article
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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 3 institutions in 1 country.

Johanna ErbaniMater Research Institute - The University of Queensland, Translational Research Institute, Woolloongabba, QL, Australia.
Joshua TayMater Research Institute - The University of Queensland, Translational Research Institute, Woolloongabba, QL, Australia.
Valerie BarbierMater Research Institute - The University of Queensland, Translational Research Institute, Woolloongabba, QL, Australia.
Jean-Pierre LevesqueMater Research Institute - The University of Queensland, Translational Research Institute, Woolloongabba, QL, Australia.
Ingrid G WinklerMater Research Institute - The University of Queensland, Translational Research Institute, Woolloongabba, QL, Australia.
Mater Research · AUUniversity of Queensland · AUTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interactions of leukemia cells with the bone marrow (BM) microenvironment is critical for disease progression and resistance to treatment. We have recently found that the vascular adhesion molecule E-(endothelial)-selectin is a key niche component that directly mediates acute myeloid leukemia (AML) chemo-resistance, revealing E-selectin as a promising therapeutic target. To understand how E-selectin promotes AML survival, we investigated the potential receptors on AML cells involved in E-selectin-mediated chemo-resistance. Using CRISPR-Cas9 gene editing to selectively suppress canonical E-selectin receptors CD44 or P-selectin glycoprotein ligand-1 (PSGL-1/CD162) from human AML cell line KG1a, we show that CD162, but not CD44, is necessary for E-selectin-mediated chemo-resistance

Indexed as

acute myeloid leukemiaadhesionbone marrow nicheschemoresistanceE-selectinPSGL-1 (CD162)

Identifiers

PMID32793603
PMCPMC7393995
OpenAlexW3044017108

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.