Evidence map›Paper›PMID 26400962›Full record

ArticleBlood2015

ATM deficiency promotes development of murine B-cell lymphomas that resemble diffuse large B-cell lymphoma in humans.

Karen S Hathcock, Hesed M Padilla-Nash, Jordi Camps, Dong-Mi Shin, Daniel Triner, Arthur L Shaffer, Robert W Maul, Seth M Steinberg, Patricia J Gearhart, Louis M Staudt and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. AHaematologica · 2024
    Article
  4. Article
  5. Article
  6. Journal of Cancer · 2022
    Article
  7. Genome instability and lymphoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

13 authors at 1 institution in 3 countries.

Karen S HathcockExperimental Immunology Branch.
Hesed M Padilla-NashGenetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD;
Jordi CampsGenetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD; Gastrointestinal and Pancreatic Oncology Group, Institut D'Investigacions Biomèdiques August Pi i Sunyer, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Barcelona, Spain;
Dong-Mi ShinLaboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD; Department of Food and Nutrition, Seoul National University, Seoul, Korea;
Daniel TrinerExperimental Immunology Branch.
Arthur L ShafferLymphoid Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD;ORCID http://orcid.org/0000-0002-2173-229X
Robert W MaulLaboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Bethesda, MD;
Seth M SteinbergBiostatistics and Data Management Section, Office of the Clinical Director, National Cancer Institute, National Institutes of Health, Bethesda, MD; and.
Patricia J GearhartLaboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Bethesda, MD;ORCID http://orcid.org/0000-0003-1975-4737
Louis M StaudtLymphoid Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD;
Herbert C MorseLaboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD;ORCID http://orcid.org/0000-0002-9331-3705
Thomas RiedGenetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD;
Richard J HodesExperimental Immunology Branch, National Institute on Aging, National Institutes of Health, Bethesda, MD.ORCID http://orcid.org/0000-0002-8142-5742
National Institutes of Health · US

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OMARY, BISHR · 1986 to 2021
$22.5M
Intratumor heterogeneity and tumor evolutionZIABC010834 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2023
$12.2M
Molecular Regulation of B-Cell Differentiation and FunctionZIAAI001024 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$8.3M
Lymphomas And Retroviral PathogenesisZIAAI000858 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$5.3M
Training in Basic and Translational Digestive SciencesT32DK094775 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHN Y KAO, LINDA C. SAMUELSON · 2012 to 2026
$3.6M
Intramural NIH HHSNIDDK NIH HHS P30 DK034933NIDDK NIH HHS T32 DK094775
6 · The paper itself

Abstract

The serine-threonine kinase ataxia-telangiectasia mutated (ATM) plays a central role in maintaining genomic integrity. In mice, ATM deficiency is exclusively associated with T-cell lymphoma development, whereas B-cell tumors predominate in human ataxia-telangiectasia patients. We demonstrate in this study that when T cells are removed as targets for lymphomagenesis and as mediators of immune surveillance, ATM-deficient mice exclusively develop early-onset immunoglobulin M(+) B-cell lymphomas that do not transplant to immunocompetent mice and that histologically and genetically resemble the activated B cell-like (ABC) subset of human diffuse large B-cell lymphoma (DLBCL). These B-cell lymphomas show considerable chromosomal instability and a recurrent genomic amplification of a 4.48-Mb region on chromosome 18 that contains Malt1 and is orthologous to a region similarly amplified in human ABC DLBCL. Of importance, amplification of Malt1 in these lymphomas correlates with their dependence on nuclear factor (NF)-κB, MALT1, and B-cell receptor (BCR) signaling for survival, paralleling human ABC DLBCL. Further, like some human ABC DLBCLs, these mouse B-cell lymphomas also exhibit constitutive BCR-dependent NF-κB activation. This study reveals that ATM protects against development of B-cell lymphomas that model human ABC DLBCL and identifies a potential role for T cells in preventing the emergence of these tumors.

Indexed as

Immunologic SurveillanceAnimalsAtaxia Telangiectasia Mutated ProteinsCaspasesCell Line, TumorChromosomal InstabilityGenetic LociHumansLymphoma, Large B-Cell, DiffuseMiceMice, KnockoutMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsNF-kappa BReceptors, Antigen, B-CellT-LymphocytesAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCaspasesMALT1 protein, humanMalt1 protein, mouseMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsNF-kappa BReceptors, Antigen, B-CellTumor Suppressor Proteins

Identifiers

PMID26400962
PMCPMC4643004
OpenAlexW2201612457

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.