Evidence map›Paper›PMID 34021249›Full record

ArticleLeukemia2021

Thyroid MALT lymphoma: self-harm to gain potential T-cell help.

Fangtian Wu, Natsuko Watanabe, Maria-Myrsini Tzioni, Ayse Akarca, Chunye Zhang, Yan Li, Zi Chen, Francesco Cucco, Natasha Carmell, Jaeduk Yoshimura Noh and 15 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Mucosa-associated lymphoid tissue lymphoma with monoclonal T-cell expansion.Virchows Archiv : an international journal of pathology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  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

25 authors at 13 institutions in 6 countries.

Fangtian WuDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Natsuko WatanabeDepartment of Internal Medicine, Ito Hospital, Tokyo, Japan.
Maria-Myrsini TzioniDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Ayse AkarcaDepartment of Pathology, University College London, London, UK.ORCID http://orcid.org/0000-0003-0629-3927
Chunye ZhangDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Yan LiDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Zi ChenDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Francesco CuccoDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Natasha CarmellIndica Labs, Albuquerque, NM, USA.
Jaeduk Yoshimura NohDepartment of Internal Medicine, Ito Hospital, Tokyo, Japan.
Koichi ItoDepartment of Surgery, Ito Hospital, Tokyo, Japan.
Rachel DobsonDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Sarah MoodyDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-4904-1041
Wenqing YaoDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Wenyan ZhangDepartment of Pathology, West China Hospital, Sichuan University, Chengdu, PR China.
Weiping LiuDepartment of Pathology, West China Hospital, Sichuan University, Chengdu, PR China.
Hongxiang LiuMolecular Malignancy Laboratory, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
Jessica OkosunCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0001-6021-5044
Andreas ChottInstitute of Pathology and Microbiology, Wilhelminenspital, Vienna, Austria.
Yingwen BiDepartment of Pathology, Eye and ENT Hospital, Fudan University, Shanghai, PR China.
Shih-Sung ChuangDepartment of Pathology, Chi-Mei Medical Centre, Tainan, Taiwan.
Markus RadererDepartment of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0002-3248-5802
Jian-Yong LiDepartment of Hematology, Pukou CLL Center, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing, PR China.
Teresa MarafiotiDepartment of Pathology, University College London, London, UK.
Ming-Qing DuDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK. mqd20@cam.ac.uk.ORCID http://orcid.org/0000-0002-1017-5045
University of Cambridge · GBIto Hospital · JPSichuan University · CNUniversity College London · GBCambridge University Hospitals NHS Foundation Trust · GBChi Mei Medical Center · TWEye & ENT Hospital of Fudan University · CNJiangsu Province Hospital · CNMedical University of Vienna · ATMRC Laboratory of Molecular Biology · GBQueen Mary University of London · GBSandia National Laboratories California · USWilhelminen Hospital · AT

Funding

Department of Health
6 · The paper itself

Abstract

The development of extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) is driven by chronic inflammatory responses and acquired genetic changes. To investigate its genetic bases, we performed targeted sequencing of 93 genes in 131 MALT lymphomas including 76 from the thyroid. We found frequent deleterious mutations of TET2 (86%), CD274 (53%), TNFRSF14 (53%), and TNFAIP3 (30%) in thyroid MALT lymphoma. CD274 was also frequently deleted, together with mutation seen in 68% of cases. There was a significant association between CD274 mutation/deletion and TNFRSF14 mutation (p = 0.001). CD274 (PD-L1) and TNFRSF14 are ligands for the co-inhibitory receptor PD1 and BTLA on T-helper cells, respectively, their inactivation may free T-cell activities, promoting their help to malignant B-cells. In support of this, both the proportion of activated T-cells (CD4+CD69+/CD4+) within the proximity of malignant B-cells, and the level of transformed blasts were significantly higher in cases with CD274/TNFRSF14 genetic abnormalities than those without these changes. Both CD274 and TNFRSF14 genetic changes were significantly associated with Hashimoto's thyroiditis (p = 0.01, p = 0.04, respectively), and CD274 mutation/deletion additionally associated with increased erythrocyte sedimentation rate (p = 0.0001). In conclusion, CD274/TNFRSF14 inactivation in thyroid MALT lymphoma B-cells may deregulate their interaction with T-cells, promoting co-stimulations and impairing peripheral tolerance.

Indexed as

B7-H1 AntigenDioxygenasesDNA-Binding ProteinsHigh-Throughput Nucleotide SequencingHumansLymphoma, B-Cell, Marginal ZoneMolecular Targeted TherapyMutationReceptors, Tumor Necrosis Factor, Member 14Thyroid NeoplasmsT-LymphocytesTumor Necrosis Factor alpha-Induced Protein 3B7-H1 AntigenCD274 protein, humanDioxygenasesDNA-Binding ProteinsReceptors, Tumor Necrosis Factor, Member 14TET2 protein, humanTNFAIP3 protein, humanTNFRSF14 protein, humanTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID34021249
PMCPMC8632687
OpenAlexW3163256611

What OpenQuestion holds

Textmetadata
LicenceTDM
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.