Evidence map›Paper›PMID 27258612›Full record

ArticleBlood cancer journal2016

Transcriptome analysis of G protein-coupled receptors in distinct genetic subgroups of acute myeloid leukemia: identification of potential disease-specific targets.

A Maiga, S Lemieux, C Pabst, V-P Lavallée, M Bouvier, G Sauvageau, J Hébert

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
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  11. Shared genetic association between inflammatory bowel disease and acute myeloid leukemia: insights from mendelian randomization and transcriptomic analyses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  15. Review
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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

7 authors at 3 institutions in 1 country.

A MaigaInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, Québec, Canada.
S LemieuxInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, Québec, Canada.
C PabstInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, Québec, Canada.
V-P LavalléeInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, Québec, Canada.
M BouvierInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, Québec, Canada.
G SauvageauInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, Québec, Canada.
J HébertInstitute for Research in Immunology and Cancer (IRIC), Université de Montréal, Montréal, Québec, Canada.
Université de Montréal · CAInstitute for Research in Immunology and Cancer · CAHôpital Maisonneuve-Rosemont · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is associated with poor clinical outcome and the development of more effective therapies is urgently needed. G protein-coupled receptors (GPCRs) represent attractive therapeutic targets, accounting for approximately 30% of all targets of marketed drugs. Using next-generation sequencing, we studied the expression of 772 GPCRs in 148 genetically diverse AML specimens, normal blood and bone marrow cell populations as well as cord blood-derived CD34-positive cells. Among these receptors, 30 are overexpressed and 19 are downregulated in AML samples compared with normal CD34-positive cells. Upregulated GPCRs are enriched in chemokine (CCR1, CXCR4, CCR2, CX3CR1, CCR7 and CCRL2), adhesion (CD97, EMR1, EMR2 and GPR114) and purine (including P2RY2 and P2RY13) receptor subfamilies. The downregulated receptors include adhesion GPCRs, such as LPHN1, GPR125, GPR56, CELSR3 and GPR126, protease-activated receptors (F2R and F2RL1) and the Frizzled family receptors SMO and FZD6. Interestingly, specific deregulation was observed in genetically distinct subgroups of AML, thereby identifying different potential therapeutic targets in these frequent AML subgroups.

Indexed as

High-Throughput Nucleotide SequencingAdultAgedAged, 80 and overAntigens, CD34Bone Marrow CellsFemaleGene Expression Regulation, NeoplasticHumansLeukemia, Myeloid, AcuteMaleMiddle AgedMolecular Targeted TherapyNeoplasm ProteinsReceptors, G-Protein-CoupledSignal TransductionAntigens, CD34Neoplasm ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID27258612
PMCPMC5141352
OpenAlexW2417787511

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.