Evidence map›Paper›PMID 25384216›Full record

Trial reportThe Journal of clinical investigation2014

GP130 activation induces myeloma and collaborates with MYC.

Tobias Dechow, Sabine Steidle, Katharina S Götze, Martina Rudelius, Kerstin Behnke, Konstanze Pechloff, Susanne Kratzat, Lars Bullinger, Falko Fend, Valeria Soberon and 14 more

Abstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Immunocompetent Mouse Models of Multiple Myeloma: Therapeutic Implications.Hematology/oncology clinics of North America · 2024
    Review
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  10. Review
  11. Chronic intermittent hypoxia enhances disease progression in myeloma-resistant mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
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  13. Review
  14. Article
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  17. Aberrantly expressed LGR4 empowers Wnt signaling in multiple myeloma by hijacking osteoblast-derived R-spondins.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

24 authors at 7 institutions in 1 country.

Tobias Dechow
Sabine Steidle
Katharina S Götze
Martina Rudelius
Kerstin Behnke
Konstanze Pechloff
Susanne Kratzat
Lars Bullinger
Falko Fend
Valeria Soberon
Nadya Mitova
Zhoulei Li
Markus Thaler
Jan Bauer
Elke Pietschmann
Corinna Albers
Rebekka Grundler
Marc Schmidt-Supprian
Jürgen Ruland
Christian Peschel
Justus Duyster
Stefan Rose-John
Florian Bassermann
Ulrich Keller
Technical University of Munich · DEHeidelberg University · DEGerman Cancer Research Center · DEKiel University · DEKlinikum rechts der Isar · DEUniversity Hospital Ulm · DEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a plasma cell neoplasm that results from clonal expansion of an Ig-secreting terminally differentiated B cell. Advanced MM is characterized by tissue damage that involves bone, kidney, and other organs and is typically associated with recurrent genetic abnormalities. IL-6 signaling via the IL-6 signal transducer GP130 has been implicated as an important driver of MM pathogenesis. Here, we demonstrated that ectopic expression of constitutively active GP130 (L-GP130) in a murine retroviral transduction-transplantation model induces rapid MM development of high penetrance. L-GP130-expressing mice recapitulated all of the characteristics of human disease, including monoclonal gammopathy, BM infiltration with lytic bone lesions, and protein deposition in the kidney. Moreover, the disease was easily transplantable and allowed different therapeutic options to be evaluated in vitro and in vivo. Using this model, we determined that GP130 signaling collaborated with MYC to induce MM and was responsible and sufficient for directing the plasma cell phenotype. Accordingly, we identified Myc aberrations in the L-GP130 MM model. Evaluation of human MM samples revealed recurrent activation of STAT3, a downstream target of GP130 signaling. Together, our results indicate that deregulated GP130 activity contributes to MM pathogenesis and that pathways downstream of GP130 activity have potential as therapeutic targets in MM.

Indexed as

AnimalsCell Line, TumorCytokine Receptor gp130FemaleHumansMaleMiceMice, Inbred BALB CMultiple MyelomaNeoplasms, ExperimentalPlasma CellsProto-Oncogene Proteins c-mycSignal TransductionSTAT3 Transcription FactorCytokine Receptor gp130IL6ST protein, humanIl6st protein, mouseMYC protein, humanMyc protein, mouseProto-Oncogene Proteins c-mycSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID25384216
PMCPMC4348946
OpenAlexW2128318157

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.