Evidence map›Paper›PMID 24912157›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Endogenous retrovirus induces leukemia in a xenograft mouse model for primary myelofibrosis.

Ioanna Triviai, Marion Ziegler, Ulla Bergholz, Andrew J Oler, Thomas Stübig, Vladimir Prassolov, Boris Fehse, Christine A Kozak, Nicolaus Kröger, Carol Stocking

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Expression signature of human endogenous retroviruses in chronic lymphocytic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Review
  4. Alopecia in Harlequin mutant mice is associated with reduced AIF protein levels and expression of retroviral elements.Mammalian genome : official journal of the International Mammalian Genome Society · 2021
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Endogenous retroviruses are associated with hippocampus-based memory impairment.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Article
  11. Article
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  13. Article
  14. Article
  15. Review
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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

10 authors at 6 institutions in 3 countries.

Ioanna TriviaiRetrovirus Pathogenesis, Heinrich Pette Institute, Leibniz Institute of Experimental Virology, 20251 Hamburg, Germany;Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany;
Marion ZieglerRetrovirus Pathogenesis, Heinrich Pette Institute, Leibniz Institute of Experimental Virology, 20251 Hamburg, Germany;
Ulla BergholzRetrovirus Pathogenesis, Heinrich Pette Institute, Leibniz Institute of Experimental Virology, 20251 Hamburg, Germany;
Andrew J OlerComputational Biology Section, Bioinformatics and Computational Biosciences Branch, and.
Thomas StübigDepartment of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany;
Vladimir PrassolovEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow 119991, Russia.
Boris FehseDepartment of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany;
Christine A KozakLaboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; and.
Nicolaus KrögerDepartment of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany;
Carol StockingRetrovirus Pathogenesis, Heinrich Pette Institute, Leibniz Institute of Experimental Virology, 20251 Hamburg, Germany; carol.stocking@hpi.uni-hamburg.de.
Leibniz Institute of Virology (LIV) · DEUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DENational Institutes of Health · USNaval Research Laboratory Information Technology DivisionRussian Academy of Sciences · RU

Funding

Genetic Aspects Of Viral Oncogenesis In Wild Mouse SpeciesZIAAI000300 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KOZAK, CHRISTINE · 2009 to 2025
$19.0M
6 · The paper itself

Abstract

The compound immunodeficiencies in nonobese diabetic (NOD) inbred mice homozygous for the Prkdc(scid) and Il2rg(null) alleles (NSG mice) permit engraftment of a wide-range of primary human cells, enabling sophisticated modeling of human disease. In studies designed to define neoplastic stem cells of primary myelofibrosis (PMF), a myeloproliferative neoplasm characterized by profound disruption of the hematopoietic microenvironment, we observed a high frequency of acute myeloid leukemia (AML) in NSG mice. AML was of mouse origin, confined to PMF-xenografted mice, and contained multiple clonal integrations of ecotropic murine leukemia virus (E-MuLV). Significantly, MuLV replication was not only observed in diseased mice, but also in nontreated NSG controls. Furthermore, in addition to the single ecotropic endogenous retrovirus (eERV) located on chromosome 11 (Emv30) in the NOD genome, multiple de novo germ-line eERV integrations were observed in mice from each of four independent NSG mouse colonies. Analysis confirmed that E-MuLV originated from the Emv30 provirus and that recombination events were not necessary for virus replication or AML induction. Pathogenicity is thus likely attributable to PMF-mediated paracrine stimulation of mouse myeloid cells, which serve as targets for retroviral infection and transformation, as evidenced by integration into the Evi1 locus, a hotspot for retroviral-induced myeloid leukemia. This study thus corroborates a role of paracrine stimulation in PMF disease progression, underlines the importance of target cell type and numbers in MuLV-induced disease, and mandates awareness of replicating MuLV in NOD immunodeficient mice, which can significantly influence experimental results and their interpretation.

Indexed as

AgedAnimalsBlotting, SouthernEndogenous RetrovirusesFemaleHumansInterleukin Receptor Common gamma SubunitLeukemia, ExperimentalLeukemia, Myeloid, AcuteLeukemia Virus, MurineMaleMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutMice, SCIDIl2rg protein, mouseInterleukin Receptor Common gamma Subunit

Identifiers

PMID24912157
PMCPMC4060668
OpenAlexW2015118659

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.