Evidence map›Paper›PMID 32193251›Full record

ArticleHaematologica2021

The process of somatic hypermutation increases polyreactivity for central nervous system antigens in primary central nervous system lymphoma.

Manuel Montesinos-Rongen, Monica Terrao, Caroline May, Katrin Marcus, Ingmar Blümcke, Martin Hellmich, Ralf Küppers, Anna Brunn, Martina Deckert

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Observational
  8. Central Nervous System Lymphoma: Novel Therapies.Current treatment options in oncology · 2022
    Review
  9. Review
  10. Article
  11. 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

9 authors at 4 institutions in 2 countries.

Manuel Montesinos-RongenInstitute of Neuropathology, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Monica TerraoInstitute of Neuropathology, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Caroline MayMedizinisches Proteom-Center, Ruhr-University Bochum, Bochum, Germany.
Katrin MarcusMedizinisches Proteom-Center, Ruhr-University Bochum, Bochum, Germany.
Ingmar BlümckeDepartment of Neuropathology, University Hospital Erlangen, Erlangen, Germany.
Martin HellmichInstitute of Medical Statistics and Computational Biology, University Hospital of Cologne, Cologne.
Ralf KüppersInstitute of Cell Biology (Cancer Research), University of Duisburg-Essen, Medical School, Essen.
Anna BrunnInstitute of Neuropathology, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Martina DeckertInstitute of Neuropathology, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
University Hospital Cologne · DERuhr University Bochum · DEUniversitätsklinikum Erlangen · DEUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immunoglobulin (Ig) heavy and light chain variable gene mutational pattern of the B cell receptor (BCR) in primary central nervous system (CNS) lymphoma (PCNSL) cells suggests antigenic selection to drive pathogenesis and confinement to the CNS. This hypothesis is supported by the observation that the tumor B cell receptor (tBCR) of PCNSL is polyreactive and may be stimulated by CNS proteins. To obtain further insight into the role of the germinal center (GC) reaction on BCR reactivity, we constructed recombinant antibodies (recAb) with Ig heavy and light chain sequences of the corresponding naive BCR (nBCR) by reverting tBCR somatic mutations in 10 PCNSL. Analysis of nBCR-derived recAb reactivity by a protein microarray and immunoprecipitation demonstrated auto- and polyreactivity in all cases. Self-/polyreactivity was not lost during the GC reaction; surprisingly, tBCR significantly increased self-/polyreactivity. In addition to proteins recognized by both the nBCR and tBCR, tBCR gained self-/polyreactivity particularly for proteins expressed in the CNS including proteins of oligodendrocytes/myelin, the S100 protein family, and splicing factors. Thus, in PCNSL pathogenesis, a faulty GC reaction may increase self-/polyreactivity, hereby facilitating BCR signaling via multiple CNS antigens, and may ultimately foster tumor cell survival in the CNS.

Indexed as

Central Nervous System NeoplasmsImmunoglobulin Heavy ChainsCentral Nervous SystemGerminal CenterHumansReceptors, Antigen, B-CellImmunoglobulin Heavy ChainsReceptors, Antigen, B-Cell

Identifiers

PMID32193251
PMCPMC7927892
OpenAlexW3011562360

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.