Evidence map›Paper›PMID 24487434›Full record

ArticleNature medicine2014

Fas ligand-mediated immune surveillance by T cells is essential for the control of spontaneous B cell lymphomas.

Shoukat Afshar-Sterle, Dimitra Zotos, Nicholas J Bernard, Anna K Scherger, Lisa Rödling, Amber E Alsop, Jennifer Walker, Frederick Masson, Gabrielle T Belz, Lynn M Corcoran and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 100 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 1 country.

Shoukat Afshar-Sterle1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia. [3].
Dimitra Zotos1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia. [3].
Nicholas J Bernard1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia. [3].
Anna K Scherger1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Lisa Rödling1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Amber E Alsop1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Jennifer Walker1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Frederick Masson1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Gabrielle T Belz1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Lynn M Corcoran1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Lorraine A O'Reilly1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Andreas Strasser1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Mark J Smyth1] Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia. [2] School of Medicine, University of Queensland, Herston, Queensland, Australia.
Ricky Johnstone1] Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia. [2] Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australia.
David M Tarlinton1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Stephen L Nutt1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Axel Kallies1] Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.
Walter and Eliza Hall Institute of Medical Research · AUPeter MacCallum Cancer Centre · AUQIMR Berghofer Medical Research Institute · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of function of the tumor suppressor gene PRDM1 (also known as BLIMP1) or deregulated expression of the oncogene BCL6 occurs in a large proportion of diffuse large B cell lymphoma (DLBCL) cases. However, targeted mutation of either gene in mice leads to only slow and infrequent development of malignant lymphoma, and despite frequent mutation of BCL6 in activated B cells of healthy individuals, lymphoma development is rare. Here we show that T cells prevent the development of overt lymphoma in mice caused by Blimp1 deficiency or overexpression of Bcl6 in the B cell lineage. Impairment of T cell control results in rapid development of DLBCL-like disease, which can be eradicated by polyclonal CD8(+) T cells in a T cell receptor-, CD28- and Fas ligand-dependent manner. Thus, malignant transformation of mature B cells requires mutations that impair intrinsic differentiation processes and permit escape from T cell-mediated tumor surveillance.

Indexed as

AnimalsB-LymphocytesCD8-Positive T-LymphocytesCell SeparationCell Transformation, NeoplasticDisease Models, AnimalDNA-Binding ProteinsFas Ligand ProteinFlow CytometryGenes, Tumor SuppressorImmunologic SurveillanceLymphoma, Large B-Cell, DiffuseMiceMice, TransgenicMutationPositive Regulatory Domain I-Binding Factor 1Bcl6 protein, mouseDNA-Binding ProteinsFas Ligand ProteinFasl protein, mousePositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseProto-Oncogene Proteins c-bcl-6Transcription Factors

Identifiers

PMID24487434
OpenAlexW1990797005

What OpenQuestion holds

Textmetadata
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.