Evidence map›Paper›PMID 28970470›Full record

ArticleNature communications2017

NFAT2 is a critical regulator of the anergic phenotype in chronic lymphocytic leukaemia.

Melanie Märklin, Jonas S Heitmann, Alexander R Fuchs, Felicia M Truckenmüller, Michael Gutknecht, Stefanie Bugl, Sebastian J Saur, Juliane Lazarus, Ursula Kohlhofer, Leticia Quintanilla-Martinez and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. A Novel Peptide that Disrupts the Lck-IPArchives of microbiology & immunology · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

19 authors at 3 institutions in 2 countries.

Melanie MärklinDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.ORCID http://orcid.org/0000-0002-2920-3894
Jonas S HeitmannDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Alexander R FuchsDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Felicia M TruckenmüllerDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Michael GutknechtDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Stefanie BuglDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Sebastian J SaurDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Juliane LazarusDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Ursula KohlhoferDepartment of Pathology, University of Tübingen, Tübingen, 72076, Germany.
Leticia Quintanilla-MartinezDepartment of Pathology, University of Tübingen, Tübingen, 72076, Germany.ORCID http://orcid.org/0000-0001-7156-5365
Hans-Georg RammenseeDepartment of Immunology, University of Tübingen, Tübingen, 72076, Germany.
Helmut R SalihDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Hans-Georg KoppDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Michael HaapDepartment of Endocrinology, Diabetology, Clinical Pathology and Metabolism, University of Tübingen, Tübingen, 72076, Germany.
Andreas KirschniakDepartment of Surgery, University of Tübingen, Tübingen, 72076, Germany.
Lothar KanzDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Anjana RaoLa Jolla Institute of Allergy and Immunology, La Jolla, CA, 92037, USA.
Stefan WirthsDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany.
Martin R MüllerDepartment of Oncology, Haematology and Immunology, University of Tübingen, Tübingen, 72076, Germany. martin.mueller@med.uni-tuebingen.de.
University of Tübingen · DEGerman Cancer Research Center · DELa Jolla Institute for Immunology · US

Funding

SIGNAL TRANSDUCTION AND GENE INDUCTION IN T LYMPHOCYTESR01AI040127 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI HOGAN, PATRICK, RAO, ANJANA · 1996 to 2025
$13.3M
NIAID NIH HHS R01 AI040127
6 · The paper itself

Abstract

Chronic lymphocytic leukaemia (CLL) is a clonal disorder of mature B cells. Most patients are characterised by an indolent disease course and an anergic phenotype of their leukaemia cells, which refers to a state of unresponsiveness to B cell receptor stimulation. Up to 10% of CLL patients transform from an indolent subtype to an aggressive form of B cell lymphoma over time (Richter´s syndrome) and show a significantly worse treatment outcome. Here we show that B cell-specific ablation of Nfat2 leads to the loss of the anergic phenotype culminating in a significantly compromised life expectancy and transformation to aggressive disease. We further define a gene expression signature of anergic CLL cells consisting of several NFAT2-dependent genes including Cbl-b, Grail, Egr2 and Lck. In summary, this study identifies NFAT2 as a crucial regulator of the anergic phenotype in CLL.NFAT2 is a transcription factor that has been linked with chronic lymphocytic leukaemia (CLL), but its functions in CLL manifestation are still unclear. Here the authors show, by analysing mouse CLL models and characterising biopsies from CLL patients, that NFAT2 is an important regulator for the anergic phenotype of CLL.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsClonal AnergyEarly Growth Response Protein 2Gene Expression Regulation, NeoplasticHumansLeukemia, Lymphocytic, Chronic, B-CellLymphocyte Specific Protein Tyrosine Kinase p56(lck)MiceNFATC Transcription FactorsPhenotypeProto-Oncogene Proteins c-cblUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingCBLB protein, humanCblb protein, mouseEarly Growth Response Protein 2EGR2 protein, humanEgr2 protein, mouseLymphocyte Specific Protein Tyrosine Kinase p56(lck)NFATC1 protein, humanNfatc1 protein, mouseNFATC Transcription FactorsProto-Oncogene Proteins c-cblRNF128 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID28970470
PMCPMC5624906
OpenAlexW2758825180

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.