Evidence map›Paper›PMID 27198204›Full record

ArticleLeukemia2016

Distinct genetic evolution patterns of relapsing diffuse large B-cell lymphoma revealed by genome-wide copy number aberration and targeted sequencing analysis.

D Juskevicius, T Lorber, J Gsponer, V Perrina, C Ruiz, F Stenner-Liewen, S Dirnhofer, A Tzankov

Abstract read
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In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. RHOA controls oncogenic B cell receptor signaling in aggressive lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  11. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Clinical significance of plasma PD-L1Annals of hematology · 2023
    Article
  16. Relapse Timing Is Associated With Distinct Evolutionary Dynamics in Diffuse Large B-Cell Lymphoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
    Article
  17. Article
  18. Relapse timing is associated with distinct evolutionary dynamics in DLBCL.medRxiv : the preprint server for health sciences · 2023
    Article
  19. Article
  20. Article
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

8 authors.

D JuskeviciusInstitute of Pathology, University Hospital Basel, Basel, Switzerland.
T LorberInstitute of Pathology, University Hospital Basel, Basel, Switzerland.
J GsponerInstitute of Pathology, University Hospital Basel, Basel, Switzerland.
V PerrinaInstitute of Pathology, University Hospital Basel, Basel, Switzerland.
C RuizInstitute of Pathology, University Hospital Basel, Basel, Switzerland.
F Stenner-LiewenDepartment of Oncology, University Hospital Basel, Basel, Switzerland.
S DirnhoferInstitute of Pathology, University Hospital Basel, Basel, Switzerland.
A TzankovInstitute of Pathology, University Hospital Basel, Basel, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recurrences of diffuse large B-cell lymphomas (DLBCL) result in significant morbidity and mortality, but their underlying genetic and biological mechanisms are unclear. Clonal relationship in DLBCL relapses so far is mostly addressed by the investigation of immunoglobulin (IG) rearrangements, therefore, lacking deeper insights into genome-wide lymphoma evolution. We studied mutations and copy number aberrations in 20 paired relapsing and 20 non-relapsing DLBCL cases aiming to test the clonal relationship between primaries and relapses to track tumors' genetic evolution and to investigate the genetic background of DLBCL recurrence. Three clonally unrelated DLBCL relapses were identified (15%). Also, two distinct patterns of genetic evolution in clonally related relapses were detected as follows: (1) early-divergent/branching evolution from a common progenitor in 6 patients (30%), and (2) late-divergent/linear progression of relapses in 11 patients (65%). Analysis of recurrent genetic events identified potential early drivers of lymphomagenesis (KMT2D, MYD88, CD79B and PIM1). The most frequent relapse-specific events were additional mutations in KMT2D and alterations of MEF2B. SOCS1 mutations were exclusive to non-relapsing DLBCL, whereas primaries of relapsing DLBCL more commonly displayed gains of 10p15.3-p12.1 containing the potential oncogenes PRKCQ, GATA3, MLLT10 and ABI1. Altogether, our study expands the knowledge on clonal relationship, genetic evolution and mutational basis of DLBCL relapses.

Indexed as

DNA Copy Number VariationsEvolution, MolecularMutationAdultAgedAged, 80 and overBase SequenceClone CellsGenome, HumanHumansLymphoma, Large B-Cell, DiffuseMiddle AgedOncogenesRecurrence

Identifiers

PMID27198204

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.