Evidence map›Paper›PMID 27063597›Full record

ArticleLeukemia2016

GPR56 contributes to the development of acute myeloid leukemia in mice.

D Daria, N Kirsten, A Muranyi, M Mulaw, S Ihme, A Kechter, M Hollnagel, L Bullinger, K Döhner, H Döhner and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

D DariaInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
N KirstenInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
A MuranyiInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
M MulawInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
S IhmeInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
A KechterInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
M HollnagelInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
L BullingerDepartment of Internal Medicine III, University Hospital of Ulm, Ulm, Germany.
K DöhnerDepartment of Internal Medicine III, University Hospital of Ulm, Ulm, Germany.
H DöhnerDepartment of Internal Medicine III, University Hospital of Ulm, Ulm, Germany.
M Feuring-BuskeDepartment of Internal Medicine III, University Hospital of Ulm, Ulm, Germany.
C BuskeInstitute for Experimental Cancer Research, Comprehensive Cancer Center, University Hospital of Ulm, Ulm, Germany.
University Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The G protein-coupled receptor 56 (GPR56) was identified as part of the molecular signature of functionally validated leukemic stem cells isolated from patients with acute myeloid leukemia (AML). This report now demonstrates particularly high expression of GPR56 in patients with mutant NPM1 and FLT3-length mutation and association of high GPR56 expression with inferior prognosis in a large patient cohort treated in two independent multicenter phase III trials. Functional relevance of GPR56 expression was validated in mice, in which co-expression of Gpr56 significantly accelerated HOXA9-induced leukemogenesis and vice versa knockdown of Gpr56 delayed onset of HOXA9/MEIS1-induced AML. Overexpression of Gpr56 grossly changed the molecular phenotype of Hoxa9-transduced cells affecting pathways involved in G protein-coupled receptors (GPRCs) and associated intracellular signaling. Blockage of surface GPR56 by an anti-GPR56 antibody successfully impaired engraftment of primary human AML cells. In summary, these data demonstrate that high expression of GPR56 is able to contribute to AML development and characterize the GPR56 as a potential novel target for antibody-mediated antileukemic strategies.

Indexed as

AnimalsCarcinogenesisFemaleHeterograftsHomeodomain ProteinsHumansLeukemia, Myeloid, AcuteMaleMiceMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsNucleophosminReceptors, G-Protein-CoupledADGRG1 protein, humanAdgrg1 protein, mousehomeobox protein HOXA9Homeodomain ProteinsMEIS1 protein, humanMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsNPM1 protein, humanNpm1 protein, mouseNucleophosminReceptors, G-Protein-Coupled

Identifiers

PMID27063597
OpenAlexW2322005850

What OpenQuestion holds

Textmetadata
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.