Evidence map›Paper›PMID 26712879›Full record

ArticleAmerican journal of clinical pathology2016

Clonality Analysis of Immunoglobulin Gene Rearrangement by Next-Generation Sequencing in Endemic Burkitt Lymphoma Suggests Antigen Drive Activation of BCR as Opposed to Sporadic Burkitt Lymphoma.

Teresa Amato, Francesco Abate, Pierpaolo Piccaluga, Michele Iacono, Chiara Fallerini, Alessandra Renieri, Giulia De Falco, Maria Raffaella Ambrosio, Vaselious Mourmouras, Martin Ogwang and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of clinical pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Reply to Chien: Clarification of the effect of ligand on γδ-TCR repertoire selection.Proceedings of the National Academy of Sciences of the United States of America · 2018
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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

16 authors at 5 institutions in 3 countries.

Teresa AmatoFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy.
Francesco AbateDepartment of Biomedical Informatics, Columbia University College of Physicians and Surgeons, New York, NY.
Pierpaolo PiccalugaHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine (DIMES), S. Orsola-Malpighi Hospital, Bologna University School of Medicine, Bologna, Italy.
Michele IaconoRoche Tissue Diagnostic & Sequencing, Roche Diagnostic S.P.A. Monza (MB), Italy.
Chiara FalleriniFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy.
Alessandra RenieriFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy.
Giulia De FalcoFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy.
Maria Raffaella AmbrosioFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy.
Vaselious MourmourasFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy.
Martin OgwangLacor Hospital, Gulu, Uganda.
Valeria CalbiLacor Hospital, Gulu, Uganda.
Roul RabadanDepartment of Biomedical Informatics, Columbia University College of Physicians and Surgeons, New York, NY.
Michael HummelInstitut Fur Pathologie, Campus Benjamin Franklin, Charitè, Universitatsmedizin, Berlin, Germany.
Stefano PileriHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine (DIMES), S. Orsola-Malpighi Hospital, Bologna University School of Medicine, Bologna, Italy.
Lorenzo LeonciniFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy lorenzo.leoncini@dbm.unisi.it.
Cristiana BellanFrom the Department of Medical Biotechnologies, University of Siena, Siena, Italy.
University of Siena · ITColumbia University · USPoliclinico S.Orsola-Malpighi · ITSt. Mary's Hospital Lacor · UGRoche (Italy) · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRecent studies using next-generation sequencing (NGS) analysis disclosed the importance of the intrinsic activation of the B-cell receptor (BCR) pathway in the pathogenesis of sporadic Burkitt lymphoma (sBL) due to mutations of TCF3/ID3 genes. Since no definitive data are available on the genetic landscape of endemic Burkitt (eBL), we first assessed the mutation frequency of TCF3/ID3 in eBL compared with sBL and subsequently the somatic hypermutation status of the BCR to answer whether an extrinsic activation of BCR signaling could also be demonstrated in Burkitt lymphoma.

methodsWe assessed the mutations of TCF3/ID3 by RNAseq and the BCR status by NGS analysis of the immunoglobulin genes (IGs).

resultsWe detected mutations of TCF3/ID3 in about 30% of the eBL cases. This rate is significantly lower than that detected in sBL (64%). The NGS analysis of IGs revealed intraclonal diversity, suggesting an active targeted somatic hypermutation process in eBL compared with sBL.

conclusionsThese findings support the view that the antigenic pressure plays a key role in the pathogenetic pathways of eBL, which may be partially distinct from those driving sBL development.

Indexed as

Genes, ImmunoglobulinAdultBasic Helix-Loop-Helix ProteinsBurkitt LymphomaChildChild, PreschoolFemaleHigh-Throughput Nucleotide SequencingHumansInfantMaleMiddle AgedMutationYoung AdultBasic Helix-Loop-Helix ProteinsTCF3 protein, humanBCRBurkitt lymphomaClonality analysisNGS

Identifiers

PMID26712879
PMCPMC4778259
OpenAlexW2203169281

What OpenQuestion holds

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Registered trials

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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.