Evidence map›Paper›PMID 20357826›Full record

ArticleLeukemia2010

EVI1 overexpression in distinct subtypes of pediatric acute myeloid leukemia.

B V Balgobind, S Lugthart, I H Hollink, S T J C M Arentsen-Peters, E R van Wering, S S N de Graaf, D Reinhardt, U Creutzig, G J L Kaspers, E S J M de Bont and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. LowFrontiers in medicine · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. HighFrontiers in oncology · 2021
    Article
  15. HighHemaSphere · 2020
    Article
  16. Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Myeloid leukemia with high EVI1 expression is sensitive to 5-aza-2'-deoxycytidine by targeting miR-9.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Article
  19. Opportunities for immunotherapy in childhood acute myeloid leukemia.Hematology. American Society of Hematology. Education Program · 2019
    Review
  20. Review
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

18 authors at 9 institutions in 3 countries.

B V BalgobindDepartment of Pediatric Oncology/Hematology, Erasmus MC--Sophia Children's Hospital, Rotterdam, The Netherlands.
S Lugthart
I H Hollink
S T J C M Arentsen-Peters
E R van Wering
S S N de Graaf
D Reinhardt
U Creutzig
G J L Kaspers
E S J M de Bont
J Stary
J Trka
M Zimmermann
H B Beverloo
R Pieters
R Delwel
C M Zwaan
M M van den Heuvel-Eibrink
Erasmus MC - Sophia Children’s Hospital · NLErasmus MC · NLCharles University · CZMedizinische Hochschule Hannover · DEAmsterdam UMC Location VUmc · NLRadboud University Medical Center · NLStichting Kinderoncologie Nederland · NLUniversity Hospital Münster · DEUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of the ecotropic virus integration-1 (EVI1) gene (EVI1+), localized at chromosome 3q26, is associated with adverse outcome in adult acute myeloid leukemia (AML). In pediatric AML, 3q26 abnormalities are rare, and the role of EVI1 is unknown. We studied 228 pediatric AML samples for EVI1+ using gene expression profiling and RQ-PCR. EVI1+ was found in 20/213 (9%) of children with de novo AML, and in 4/8 with secondary AML. It was predominantly found in MLL-rearranged AML (13/47), monosomy 7 (2/3), or FAB M6/7 (6/10), and mutually exclusive with core-binding factor AML, t(15;17), and NPM1 mutations. Fluorescent in situ hybridization (FISH) was performed to detect cryptic 3q26 abnormalities. However, none of the EVI1+ patients harbored structural 3q26 alterations. Although significant differences in 4 years pEFS for EVI1+ and EVI1- pediatric AML were observed (28%+/-11 vs 44%+/-4, P=0.04), multivariate analysis did not identify EVI1+ as an independent prognostic factor. We conclude that EVI1+ can be found in approximately 10% of pediatric AML. Although EVI1+ was not an independent prognostic factor, it was predominantly found in subtypes of pediatric AML that are related with an intermediate to unfavorable prognosis. Further research should explain the role of EVI1+ in disease biology in these cases. Remarkably, no 3q26 abnormalities were identified in EVI1+ pediatric AML.

Indexed as

Gene Expression Regulation, LeukemicBiomarkers, TumorChildChild, PreschoolChromosome AberrationsChromosomes, Human, Pair 3DNA-Binding ProteinsFemaleGene Expression ProfilingHumansIn Situ Hybridization, FluorescenceLeukemia, Myeloid, AcuteMaleMDS1 and EVI1 Complex Locus ProteinNucleophosminOligonucleotide Array Sequence AnalysisBiomarkers, TumorDNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanNPM1 protein, humanNucleophosminRNA, MessengerTranscription Factors

Identifiers

PMID20357826
OpenAlexW2112362958

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.