Evidence map›Paper›PMID 25331116›Full record

ArticleBlood2015

EVI1-rearranged acute myeloid leukemias are characterized by distinct molecular alterations.

Vincent-Philippe Lavallée, Patrick Gendron, Sébastien Lemieux, Giovanni D'Angelo, Josée Hébert, Guy Sauvageau

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.3field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Vincent-Philippe LavalléeThe Leucegene Project at the Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada; Division of Hematology, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada;
Patrick GendronThe Leucegene Project at the Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada;
Sébastien LemieuxThe Leucegene Project at the Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada; Computer Science and Operation Research, Université de Montréal, Montréal, QC, Canada;
Giovanni D'AngeloBanque de Cellules Leucémiques du Québec, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada; and.
Josée HébertThe Leucegene Project at the Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada; Division of Hematology, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada; Banque de Cellules Leucémiques du Québec, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada; and Department of Medicine, Faculty of Medicine, Université de Montréal, QC, Canada.
Guy SauvageauThe Leucegene Project at the Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, QC, Canada; Division of Hematology, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada; Banque de Cellules Leucémiques du Québec, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada; and Department of Medicine, Faculty of Medicine, Université de Montréal, QC, 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

The genetic and transcriptional signature of EVI1 (ecotropic viral integration site 1)-rearranged (EVI1-r) acute myeloid leukemias (AMLs) remains poorly defined. We performed RNA sequencing of 12 EVI1-r AMLs and compared the results with those of other AML subtypes (n = 139) and normal CD34(+) cells (n = 17). Results confirm high frequencies of RAS and other activated signaling mutations (10/12 AMLs) and identify new recurrent mutations in splicing factors (5/12 AMLs in SF3B1 and 2/12 AMLs in U2AF1), IKZF1 (3/12 AMLs), and TP53 (3/12 AMLs). Mutations in IKZF1, a gene located on chromosome 7, and monosomy 7 are mutually exclusive in this disease. Moreover IKZF1 expression is halved in monosomy 7 leukemias. EVI-r AMLs are also characterized by a unique transcriptional signature with high expression levels of MECOM, PREX2, VIP, MYCT1, and PAWR. Our results suggest that EVI1-r AMLs could be molecularly defined by specific transcriptomic anomalies and a hitherto unseen mutational pattern. Larger patient cohorts will better determine the frequency of these events.

Indexed as

Gene Expression Regulation, LeukemicMutationApoptosis Regulatory ProteinsChromosomes, Human, Pair 7DNA-Binding ProteinsGene Expression ProfilingGuanine Nucleotide Exchange FactorsHumansIkaros Transcription FactorLeukemia, Myeloid, AcuteMDS1 and EVI1 Complex Locus ProteinNuclear ProteinsProto-OncogenesSignal TransductionTranscription FactorsTranscriptomeApoptosis Regulatory ProteinsDNA-Binding ProteinsGuanine Nucleotide Exchange FactorsIkaros Transcription FactorIKZF1 protein, humanMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMYCT1 protein, humanNuclear ProteinsPREX2 protein, humanprostate apoptosis response-4 proteinTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53Vasoactive Intestinal Peptide

Identifiers

PMID25331116
PMCPMC4358966
OpenAlexW2029477694

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.