Evidence map›Paper›PMID 25117979›Full record

ArticleNeoplasia (New York, N.Y.)2014

SAMSN1 is a tumor suppressor gene in multiple myeloma.

Jacqueline E Noll, Duncan R Hewett, Sharon A Williams, Kate Vandyke, Chung Kok, Luen B To, Andrew C W Zannettino

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-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

34 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Immunocompetent Mouse Models of Multiple Myeloma: Therapeutic Implications.Hematology/oncology clinics of North America · 2024
    Review
  10. Molecular Mechanisms of IL18 in Disease.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 3 institutions in 1 country.

Jacqueline E NollMyeloma Research Laboratory, School of Medical Sciences, Faculty of Health Science, University of Adelaide, Adelaide, Australia; Department of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia.
Duncan R HewettMyeloma Research Laboratory, School of Medical Sciences, Faculty of Health Science, University of Adelaide, Adelaide, Australia; Department of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia.
Sharon A WilliamsMyeloma Research Laboratory, School of Medical Sciences, Faculty of Health Science, University of Adelaide, Adelaide, Australia; Department of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia.
Kate VandykeMyeloma Research Laboratory, School of Medical Sciences, Faculty of Health Science, University of Adelaide, Adelaide, Australia; Department of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia.
Chung KokAcute Myeloid Leukaemia Laboratory, Department of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia.
Luen B ToDepartment of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia.
Andrew C W ZannettinoMyeloma Research Laboratory, School of Medical Sciences, Faculty of Health Science, University of Adelaide, Adelaide, Australia; Department of Haematology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia. Electronic address: andrew.zannettino@adelaide.edu.au.
South Australia Pathology · AUCentre for Cancer Biology · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM), a hematological malignancy characterized by the clonal growth of malignant plasma cells (PCs) in the bone marrow, is preceded by the benign asymptomatic condition, monoclonal gammopathy of undetermined significance (MGUS). Several genetic abnormalities have been identified as critical for the development of MM; however, a number of these abnormalities are also found in patients with MGUS, indicating that there are other, as yet unidentified, factors that contribute to the onset of MM disease. In this study, we identify a Samsn1 gene deletion in the 5TGM1/C57BL/KaLwRij murine model of myeloma. In addition, SAMSN1 expression is reduced in the malignant CD138+ PCs of patients with MM and this reduced expression correlates to total PC burden. We identify promoter methylation as a potential mechanism through which SAMSN1 expression is modulated in human myeloma cell lines. Notably, re-expression of Samsn1 in the 5TGM1 murine PC line resulted in complete inhibition of MM disease development in vivo and decreased proliferation in stromal cell-PC co-cultures in vitro. This is the first study to identify deletion of a key gene in the C57BL/KaLwRij mice that also displays reduced gene expression in patients with MM and is therefore likely to play an integral role in MM disease development.

Indexed as

Genes, Tumor SuppressorAdaptor Proteins, Vesicular TransportAlternative SplicingAnimalsCell Line, TumorChromosome MappingDisease Models, AnimalDisease ProgressionDNA MethylationDNA Mutational AnalysisFemaleGene DeletionGene ExpressionGene Expression ProfilingGene OrderGenetic LociAdaptor Proteins, Vesicular TransportSAMSN1 protein, humanSLy2 protein, mouse

Identifiers

PMID25117979
PMCPMC4198825
OpenAlexW2072667602

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.