Evidence map›Paper›PMID 24063430›Full record

ArticleGenome biology2013

Genome-wide signatures of differential DNA methylation in pediatric acute lymphoblastic leukemia.

Jessica Nordlund, Christofer L Bäcklin, Per Wahlberg, Stephan Busche, Eva C Berglund, Maija-Leena Eloranta, Trond Flaegstad, Erik Forestier, Britt-Marie Frost, Arja Harila-Saari and 12 more

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed, 4 pooled it
7.3field-weighted citation impact, top 2% 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

226 citing papers in PubMed, 4 syntheses or guidelines pooled it, 400 citations in OpenAlex.

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  8. Gene-Temperature Interactions and Risk of Childhood Acute Lymphoblastic Leukemia.medRxiv : the preprint server for health sciences · 2026
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166 more citing papers are in PubMed but not listed here.

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

22 authors at 8 institutions in 6 countries.

Jessica Nordlund
Christofer L Bäcklin
Per Wahlberg
Stephan Busche
Eva C Berglund
Maija-Leena Eloranta
Trond Flaegstad
Erik Forestier
Britt-Marie Frost
Arja Harila-Saari
Mats Heyman
Olafur G Jónsson
Rolf Larsson
Josefine Palle
Lars Rönnblom
Kjeld Schmiegelow
Daniel Sinnett
Stefan Söderhäll
Tomi Pastinen
Mats G Gustafsson
Gudmar Lönnerholm
Ann-Christine Syvänen
Uppsala University · SENordic Society for Pediatric Hematology and Oncology · SEMcGill University · CAKarolinska University Hospital · SENational University Hospital of Iceland · ISRigshospitalet · DKUniversité de Montréal · CAUniversity Hospital of North Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough aberrant DNA methylation has been observed previously in acute lymphoblastic leukemia (ALL), the patterns of differential methylation have not been comprehensively determined in all subtypes of ALL on a genome-wide scale. The relationship between DNA methylation, cytogenetic background, drug resistance and relapse in ALL is poorly understood.

resultsWe surveyed the DNA methylation levels of 435,941 CpG sites in samples from 764 children at diagnosis of ALL and from 27 children at relapse. This survey uncovered four characteristic methylation signatures. First, compared with control blood cells, the methylomes of ALL cells shared 9,406 predominantly hypermethylated CpG sites, independent of cytogenetic background. Second, each cytogenetic subtype of ALL displayed a unique set of hyper- and hypomethylated CpG sites. The CpG sites that constituted these two signatures differed in their functional genomic enrichment to regions with marks of active or repressed chromatin. Third, we identified subtype-specific differential methylation in promoter and enhancer regions that were strongly correlated with gene expression. Fourth, a set of 6,612 CpG sites was predominantly hypermethylated in ALL cells at relapse, compared with matched samples at diagnosis. Analysis of relapse-free survival identified CpG sites with subtype-specific differential methylation that divided the patients into different risk groups, depending on their methylation status.

conclusionsOur results suggest an important biological role for DNA methylation in the differences between ALL subtypes and in their clinical outcome after treatment.

Indexed as

Chromosome AberrationsDNA MethylationGenome, HumanAdolescentAntineoplastic AgentsChildChild, PreschoolChromatinCpG IslandsDisease-Free SurvivalEnhancer Elements, GeneticFemaleGene Expression ProfilingGenome-Wide Association StudyHumansMaleAntineoplastic AgentsChromatin

Identifiers

PMID24063430
PMCPMC4014804
OpenAlexW2137147070

What OpenQuestion holds

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LicenceCC BY
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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.