Evidence map›Paper›PMID 20018915›Full record

ArticleBlood2010

IL-6 and MYC collaborate in plasma cell tumor formation in mice.

Sebastian Rutsch, Vishala T Neppalli, Dong-Mi Shin, Wendy DuBois, Herbert C Morse, Hartmut Goldschmidt, Siegfried Janz

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. SAE1 promotes tumor cell malignancyActa pharmaceutica Sinica. B · 2025
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  4. Review
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  6. Article
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  11. Chronic intermittent hypoxia enhances disease progression in myeloma-resistant mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Transgenic mouse model of IgMBlood cancer journal · 2016
    Article
  17. Article
  18. Article
  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

7 authors at 4 institutions in 2 countries.

Sebastian RutschMedizinische Klinik V, University of Heidelberg, and National Center for Tumor Diseases, Heidelberg, Germany.
Vishala T Neppalli
Dong-Mi Shin
Wendy DuBois
Herbert C Morse
Hartmut Goldschmidt
Siegfried Janz
National Center for Tumor Diseases · DENational Institutes of Health · USUniversity of Iowa · USNational Cancer Institute · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Douglas Robert Spitz · 2000 to 2026
$70.0M
The Role of Monocytes in non-Hodgkin LymphomaP50CA097274 · NCI · UNIVERSITY OF IOWA · PI WEINER, GEORGE J. · 2002 to 2021
$45.7M
Animal Model and Genotyping Core Support FacilityZICBC011047 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DU BOIS DE VROYLANDE, WENDY · 2009 to 2025
$23.1M
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
Intramural NIH HHSNCI NIH HHS P30 CA086862NCI NIH HHS P50 CA097274NCI NIH HHS P50CA097274
6 · The paper itself

Abstract

Interleukin-6 (IL-6) plays a critical role in the natural history of human plasma cell neoplasms (PCNs), such as plasma cell myeloma and plasmacytoma (PCT). IL-6 is also at the center of neoplastic plasma cell transformation in BALB/c (C) mice carrying a transgene, H2-L(d)-IL6, that encodes human IL-6 under control of the major histocompatibility complex H2-L(d) promoter: strain C.H2-L(d)-IL6. These mice are prone to PCT, but tumor development is incomplete with long latencies ( approximately 40% PCT at 12 months of age). To generate a more robust mouse model of IL-6-dependent PCN, we intercrossed strain C.H2-L(d)-IL6 with strains C.iMyc(Emu) or C.iMyc(Calpha), 2 interrelated gene-insertion models of the chromosomal T(12;15) translocation causing deregulated expression of Myc in mouse PCT. Deregulation of MYC is also a prominent feature of human PCN. We found that double-transgenic C.H2-L(d)-IL6/iMyc(Emu) and C.H2-L(d)-IL6/iMyc(Calpha) mice develop PCT with full penetrance (100% tumor incidence) and short latencies (3-6 months). The mouse tumors mimic molecular hallmarks of their human tumor counterparts, including elevated IL-6/Stat3/Bcl-X(L) signaling. The newly developed mouse strains may provide a good preclinical research tool for the design and testing of new approaches to target IL-6 in treatment and prevention of human PCNs.

Indexed as

Genes, mycAnimalsAntibodies, MonoclonalDisease Models, AnimalGene Expression ProfilingHumansHyperplasiaInterleukin-6MiceMice, TransgenicNeoplasm TransplantationPlasma CellsPlasmacytomaSignal TransductionTranslocation, GeneticAntibodies, MonoclonalIL6 protein, humanInterleukin-6

Identifiers

PMID20018915
PMCPMC2832814
OpenAlexW1996660822

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.