Evidence map›Paper›PMID 29335468›Full record

ArticleNature communications2018

AICDA drives epigenetic heterogeneity and accelerates germinal center-derived lymphomagenesis.

Matt Teater, Pilar M Dominguez, David Redmond, Zhengming Chen, Daisuke Ennishi, David W Scott, Luisa Cimmino, Paola Ghione, Jayanta Chaudhuri, Randy D Gascoyne and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

54 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
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  15. Pineocytoma in a child with Pallister-Killian syndrome: a case report and review of the literature.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
  16. Methylation of T and B Lymphocytes in Autoimmune Rheumatic Diseases.Clinical reviews in allergy & immunology · 2024
    Review
  17. Article
  18. Article
  19. The pathobiology of follicular lymphoma.Journal of clinical and experimental hematopathology : JCEH · 2023
    Article
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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

15 authors at 7 institutions in 4 countries.

Matt TeaterDepartment of Medicine, Division of Hematology and Medical Oncology, Weill Cornell Medicine, New York, NY, 10021, USA.
Pilar M DominguezDepartment of Medicine, Division of Hematology and Medical Oncology, Weill Cornell Medicine, New York, NY, 10021, USA.
David RedmondInstitute for Computational Biomedicine, Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, 10021, USA.
Zhengming ChenDivision of Biostatistics and Epidemiology, Weill Cornell Medicine, New York, NY, 10021, USA.
Daisuke EnnishiCentre for Lymphoid Cancer, British Columbia Cancer Agency, Vancouver, BC V5Z 4E6, Canada.
David W ScottCentre for Lymphoid Cancer, British Columbia Cancer Agency, Vancouver, BC V5Z 4E6, Canada.
Luisa CimminoDepartment of Pathology, Laura and Isaac Perlmutter Cancer Center, and The Helen L. and Martin S. Kimmel Center for Stem Cell Biology, NYU School of Medicine, New York, NY, 10016, USA.
Paola GhioneDepartment of Medicine, Division of Hematology and Medical Oncology, Weill Cornell Medicine, New York, NY, 10021, USA.
Jayanta ChaudhuriImmunology Program, Memorial Sloan-Kettering Cancer Center, Gerstner Sloan-Kettering Graduate School, New York, NY, 10021, USA.
Randy D GascoyneDepartment of Pathology, British Columbia Cancer Agency, Vancouver, BC V5Z 4E6, Canada.
Iannis AifantisDepartment of Pathology, Laura and Isaac Perlmutter Cancer Center, and The Helen L. and Martin S. Kimmel Center for Stem Cell Biology, NYU School of Medicine, New York, NY, 10016, USA.
Giorgio InghiramiPathology and Laboratory Medicine Department, Weill Cornell Medicine, New York, NY, 10021, USA.
Olivier ElementoInstitute for Computational Biomedicine, Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, 10021, USA. ole2001@med.cornell.edu.
Ari MelnickDepartment of Medicine, Division of Hematology and Medical Oncology, Weill Cornell Medicine, New York, NY, 10021, USA. amm2014@med.cornell.edu.
Rita ShaknovichDepartment of Medicine, Division of Hematology and Medical Oncology, Weill Cornell Medicine, New York, NY, 10021, USA. rshaknovich@gmail.com.
Cornell University · USBC Cancer Agency · CAWeill Cornell Medicine · USCancer Genetics (United States) · USMemorial Sloan Kettering Cancer Center · USNew York University · USNYU Langone’s Laura and Isaac Perlmutter Cancer Center

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
The identification and validation of mechanisms and biomarkers for relapse in diffuse large B-cell lymphoma (Administrative Supplement)R01CA194547 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI ELEMENTO, OLIVIER, TAM, WAYNE · 2015 to 2019
$2.6M
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA194547
6 · The paper itself

Abstract

Epigenetic heterogeneity is emerging as a feature of tumors. In diffuse large B-cell lymphoma (DLBCL), increased cytosine methylation heterogeneity is associated with poor clinical outcome, yet the underlying mechanisms remain unclear. Activation-induced cytidine deaminase (AICDA), an enzyme that mediates affinity maturation and facilitates DNA demethylation in germinal center (GC) B cells, is required for DLBCL pathogenesis and linked to inferior outcome. Here we show that AICDA overexpression causes more aggressive disease in BCL2-driven murine lymphomas. This phenotype is associated with increased cytosine methylation heterogeneity, but not with increased AICDA-mediated somatic mutation burden. Reciprocally, the cytosine methylation heterogeneity characteristic of normal GC B cells is lost upon AICDA depletion. These observations are relevant to human patients, since DLBCLs with high AICDA expression manifest increased methylation heterogeneity vs. AICDA-low DLBCLs. Our results identify AICDA as a driver of epigenetic heterogeneity in B-cell lymphomas with potential significance for other tumors with aberrant expression of cytidine deaminases.

Indexed as

Epigenesis, GeneticAICDA (Activation-Induced Cytidine Deaminase)AnimalsB-LymphocytesCytidine DeaminaseGene Expression ProfilingGene Expression Regulation, NeoplasticGerminal CenterHumansLymphoma, Large B-Cell, DiffuseMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicMutationAICDA (Activation-Induced Cytidine Deaminase)Cytidine Deaminase

Identifiers

PMID29335468
PMCPMC5768781
OpenAlexW2783139678

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.