Evidence map›Paper›PMID 30301958›Full record

ArticleScientific reports2018

The genetic landscape of 5T models for multiple myeloma.

Ken Maes, Bram Boeckx, Philip Vlummens, Kim De Veirman, Eline Menu, Karin Vanderkerken, Diether Lambrechts, Elke De Bruyne

Abstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Immunocompetent Mouse Models of Multiple Myeloma: Therapeutic Implications.Hematology/oncology clinics of North America · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
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

8 authors.

Ken MaesDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussel, Brussel, 1090, Belgium. kemaes@vub.ac.be.ORCID http://orcid.org/0000-0001-8906-2790
Bram BoeckxLaboratory for Translational Genetics, Department of Human Genetics, Katholieke Universiteit Leuven, VIB Center for Cancer Biology, Leuven, 3000, Belgium.
Philip VlummensDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussel, Brussel, 1090, Belgium.
Kim De VeirmanDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussel, Brussel, 1090, Belgium.
Eline MenuDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussel, Brussel, 1090, Belgium.ORCID http://orcid.org/0000-0002-0805-6581
Karin VanderkerkenDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussel, Brussel, 1090, Belgium.
Diether LambrechtsLaboratory for Translational Genetics, Department of Human Genetics, Katholieke Universiteit Leuven, VIB Center for Cancer Biology, Leuven, 3000, Belgium.
Elke De BruyneDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussel, Brussel, 1090, Belgium.ORCID http://orcid.org/0000-0003-4012-4617

Funding

Fonds Wetenschappelijk Onderzoek (Research Foundation Flanders) 12E3816NFonds Wetenschappelijk Onderzoek (Research Foundation Flanders) 12I0917NFonds Wetenschappelijk Onderzoek (Research Foundation Flanders) 1507917N
6 · The paper itself

Abstract

Murine models for multiple myeloma (MM) are often used to investigate pathobiology of multiple myeloma and disease progression. Unlike transgenic mice models, where it is known which oncogene is driving MM disease, the somatic aberrations of spontaneous syngeneic 5T models of MM have not yet been reported. Here, we analyzed the copy-number alterations (CNA) and mutational landscape of 5T2, 5T33vv and 5TGM1 murine MM models using whole-genome and whole-exome sequencing. Forty four percent of the genome of 5T2 cells is affected by CNAs while this was only 11% and 17% for 5T33vv and 5TGM1 cells, respectively. We found that up to 69% of the genes linked to gain of 1q or deletion of 13q in MM patients are present as respectively gains in 5T2 cells or deletions in 5T33 and 5TGM1 cells. Exome sequencing furthermore revealed mutations of genes involved in RAS/MAPK, PI3K/AKT1 and JAK/STAT signaling, DNA damage response, cell cycle, epigenetic regulation and extracellular matrix organization. We observed a statistically significant overlap of genes mutated in the 5T models and MM patients. Overall, the genetic landscape of the 5T models is heterogeneous with a high number of aberrations involving genes in various multiple myeloma-related pathways.

Indexed as

Genetic Predisposition to DiseaseAnimalsChromosome AberrationsDNA Copy Number VariationsEpigenesis, GeneticExtracellular MatrixGenetic Association StudiesHumansIntercellular Signaling Peptides and ProteinsMiceMitogen-Activated Protein KinasesMultiple MyelomaMutationPhosphatidylinositol 3-KinasesSignal TransductionIntercellular Signaling Peptides and ProteinsMitogen-Activated Protein KinasesPhosphatidylinositol 3-Kinases

Identifiers

PMID30301958
PMCPMC6177465

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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.