Evidence map›Paper›PMID 29052597›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2018

SYK expression in monomorphic epitheliotropic intestinal T-cell lymphoma.

Grit Mutzbauer, Katja Maurus, Clara Buszello, Jordan Pischimarov, Sabine Roth, Andreas Rosenwald, Andreas Chott, Eva Geissinger

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Extranodal T- and NK-cell lymphomas.Virchows Archiv : an international journal of pathology · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Advances in targeted therapy for malignant lymphoma.Signal transduction and targeted therapy · 2020
    Review
  18. Review
  19. 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 at 3 institutions in 2 countries.

Grit MutzbauerInstitute of Pathology, University of Wuerzburg, Wuerzburg, Germany.
Katja MaurusInstitute of Pathology, University of Wuerzburg, Wuerzburg, Germany.
Clara BuszelloInstitute of Pathology, University of Wuerzburg, Wuerzburg, Germany.
Jordan PischimarovInstitute of Pathology, University of Wuerzburg, Wuerzburg, Germany.
Sabine RothInstitute of Pathology, University of Wuerzburg, Wuerzburg, Germany.
Andreas RosenwaldInstitute of Pathology, University of Wuerzburg, Wuerzburg, Germany.
Andreas ChottInstitute of Pathology and Microbiology, Wilhelminenspital, Vienna, Austria.
Eva GeissingerInstitute of Pathology, University of Wuerzburg, Wuerzburg, Germany.
University of Würzburg · DEComprehensive Cancer Center Mainfranken · DEWilhelminen Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL), formerly known as type II enteropathy associated T-cell lymphoma (type II EATL), is a rare, aggressive primary intestinal T-cell lymphoma with a poor prognosis and an incompletely understood pathogenesis. We collected 40 cases of MEITL and 27 cases of EATL, formerly known as type I EATL, and comparatively investigated the T-cell receptor (TCR) itself and associated signaling molecules using immunohistochemistry, amplicon deep sequencing and bisulfite pyrosequencing. The TCR showed both an αβ-T-cell origin (30%) and a γδ-T-cell derivation (55%) resulting in a predominant positive TCR phenotype in MEITL compared with the mainly silent TCR phenotype in EATL (65%). The immunohistochemical expression of the spleen tyrosine kinase (SYK) turned out to be a distinctive feature of MEITL (95%) compared with EATL (0%). Aberrant SYK overexpression in MEITL is likely caused by hypomethylation of the SYK promoter, while no common mutations in the SYK gene or in its promoter could be detected. Using amplicon deep sequencing, mutations in DNMT3A, IDH2, and TET2 were infrequent events in MEITL and EATL. Immunohistochemical expression of linker for activation of T-cells (LAT) subdivided MEITL into a LAT expressing subset (33%) and a LAT silent subset (67%) with a potentially earlier disease onset in LAT-positive MEITL.

Indexed as

Adaptor Proteins, Signal TransducingAdultAgedAged, 80 and overBiomarkers, TumorDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AEnteropathy-Associated T-Cell LymphomaFemaleHumansImmunohistochemistryIsocitrate DehydrogenaseMaleMembrane ProteinsAdaptor Proteins, Signal TransducingBiomarkers, TumorDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanIDH2 protein, humanIsocitrate DehydrogenaseLAT protein, humanMembrane ProteinsProto-Oncogene ProteinsReceptors, Antigen, T-CellSyk KinaseSYK protein, humanTET2 protein, human

Identifiers

PMID29052597
OpenAlexW2765176485

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.