Evidence map›Paper›PMID 20823134›Full record

ArticleHaematologica2010

Detection of genomic aberrations in molecularly defined Burkitt's lymphoma by array-based, high resolution, single nucleotide polymorphism analysis.

René Scholtysik, Markus Kreuz, Wolfram Klapper, Birgit Burkhardt, Alfred C Feller, Michael Hummel, Markus Loeffler, Maciej Rosolowski, Carsten Schwaenen, Rainer Spang and 9 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-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

25 citing papers in PubMed, 76 citations in OpenAlex.

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  8. Cryptic insertion ofHaematologica · 2020
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  10. Review
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  12. Review
  13. A comprehensive flow-cytometry-based immunophenotypic characterization of Burkitt-like lymphoma with 11q aberration.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Article
  14. Current understanding of the role and regulation of miRNAs in Burkitt lymphoma.Blood and lymphatic cancer : targets and therapy · 2018
    Review
  15. Article
  16. 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

19 authors at 12 institutions in 5 countries.

René ScholtysikInstitute of Cell Biology (Cancer Research), University of Duisburg-Essen, Medical School, Virchowstr. 173, 45122 Essen, Germany.
Markus Kreuz
Wolfram Klapper
Birgit Burkhardt
Alfred C Feller
Michael Hummel
Markus Loeffler
Maciej Rosolowski
Carsten Schwaenen
Rainer Spang
Harald Stein
Christoph Thorns
Lorenz Trümper
Inga Vater
Swen Wessendorf
Thorsten Zenz
Reiner Siebert
Ralf Küppers
Molecular Mechanisms in Malignant Lymphomas Network Project of Deutsche Krebshilfe
University Hospital Ulm · DEUniversity of Lübeck · DEInstitute for Medical Informatics and Biostatistics · CHCharité - Universitätsmedizin Berlin · DEEssen University Hospital · DEFranklin University · USInstitute of Cell Biology · UAKiel University · DELeipzig University · DEUniversitätsmedizin Göttingen · DEUniversity Hospital Schleswig-Holstein · DEUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKnowledge about the genetic lesions that occur in Burkitt's lymphoma, besides the pathognomonic IG-MYC translocations, is limited. DESIGN AND

methodsThirty-nine molecularly-defined Burkitt's lymphomas were analyzed with high-resolution single-nucleotide polymorphism chips for genomic imbalances and uniparental disomy. Imbalances were correlated to expression profiles and selected micro-RNA analysis. Translocations affecting the MYC locus were studied by fluorescence in situ hybridization.

resultsWe detected 528 copy number changes, defining 29 recurrently imbalanced regions. Five hundred and eighteen regions of uniparental disomy were found, but these were rarely recurrent. Combined imbalance mapping and expression profiling revealed a strong correlation between copy number and expression. Several recurrent imbalances affected the MYC pathway: the micro-RNA-supercluster 17-92 was frequently gained and the transcription factor E2F2 was recurrently deleted. Molecular Burkitt's lymphoma lacking MYC translocations showed MYC gains. Amplifications of the polymerase iota gene were associated with increased frequency of positions scored as aberrant.

conclusionsThe present findings suggest that uniparental disomies do not play a major role in the pathogenesis of Burkitt's lymphoma, whereas some genes may contribute to the development of this lymphoma through gene dosage effects. Amplifications of the polymerase iota gene may be functionally linked with increased genomic alterations in Burkitt's lymphoma. The pattern and rarity of chromosomal changes detectable, even at the high resolution employed here, together with aberrations of genes regulating MYC activity, support the hypothesis that deregulation of the MYC pathway is the major force driving the pathogenesis of Burkitt's lymphoma, but show that this deregulation is more complex than previously known.

Indexed as

Chromosome AberrationsPolymorphism, Single NucleotideBurkitt LymphomaE2F2 Transcription FactorGene DosageGene Expression Regulation, NeoplasticGene RearrangementGenes, ImmunoglobulinGenome, HumanGenotypeHumansIn Situ Hybridization, FluorescenceLoss of HeterozygosityMicroRNAsOligonucleotide Array Sequence AnalysisProto-Oncogene Proteins c-mycE2F2 protein, humanE2F2 Transcription FactorMicroRNAsProto-Oncogene Proteins c-myc

Identifiers

PMID20823134
PMCPMC2995562
OpenAlexW2125605285

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.