Evidence map›Paper›PMID 28369102›Full record

ArticlePloS one2017

Abnormal repression of SHP-1, SHP-2 and SOCS-1 transcription sustains the activation of the JAK/STAT3 pathway and the progression of the disease in multiple myeloma.

Asma Beldi-Ferchiou, Nour Skouri, Cyrine Ben Ali, Ines Safra, Abderrahman Abdelkefi, Saloua Ladeb, Karima Mrad, Tarek Ben Othman, Mélika Ben Ahmed

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. 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
3.9field-weighted citation impact, top 6% 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, 41 citations in OpenAlex.

  1. Current Evidence on the Potential Role of EndothelialReviews in cardiovascular medicine · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Genetic Abnormalities in Extramedullary Multiple Myeloma.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. A comprehensive review of SHP2 and its role in cancer.Cellular oncology (Dordrecht, Netherlands) · 2022
    Review
  11. Pathogenic signaling in multiple myeloma.Seminars in oncology · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  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

9 authors at 2 institutions in 1 country.

Asma Beldi-FerchiouInstitut Pasteur de Tunis, Laboratory of Clinical Immunology, Tunis, Tunisia.ORCID http://orcid.org/0000-0002-7806-9687
Nour SkouriInstitut Pasteur de Tunis, Laboratory of Clinical Immunology, Tunis, Tunisia.
Cyrine Ben AliInstitut Pasteur de Tunis, Laboratory of Clinical Immunology, Tunis, Tunisia.
Ines SafraInstitut Pasteur de Tunis, Laboratory of Molecular and Cellular Hematology, Tunis, Tunisia.
Abderrahman AbdelkefiBone Marrow Transplantation Center, Tunis, Tunisia.
Saloua LadebUniversité de Tunis El Manar, Faculté de Médecine de Tunis, Tunis, Tunisie.
Karima MradUniversité de Tunis El Manar, Faculté de Médecine de Tunis, Tunis, Tunisie.
Tarek Ben OthmanUniversité de Tunis El Manar, Faculté de Médecine de Tunis, Tunis, Tunisie.
Mélika Ben AhmedInstitut Pasteur de Tunis, Laboratory of Clinical Immunology, Tunis, Tunisia.
Tunis University · TNInstitut Pasteur de Tunis · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sustained activation of JAK/STAT3 signaling pathway is classically described in Multiple Myeloma (MM). One explanation could be the silencing of the JAK/STAT suppressor genes, through the hypermethylation of SHP-1 and SOCS-1, previously demonstrated in MM cell lines or in whole bone marrow aspirates. The link between such suppressor gene silencing and the degree of bone marrow invasion or the treatment response has not been evaluated in depth. Using real-time RT-PCR, we studied the expression profile of three JAK/STAT suppressor genes: SHP-1, SHP-2 and SOCS-1 in plasma cells freshly isolated from the bone marrows of MM patients and healthy controls. Our data demonstrated an abnormal repression of such genes in malignant plasma cells and revealed a significant correlation between such defects and the sustained activation of the JAK/STAT3 pathway during MM. The repressed expression of SHP-1 and SHP-2 correlated significantly with a high initial degree of bone marrow infiltration but was, unexpectedly, associated with a better response to the induction therapy. Collectively, our data provide new evidences that substantiate the contribution of JAK/STAT suppressor genes in the pathogenesis of MM. They also highlight the possibility that the decreased gene expression of SHP-1 and SHP-2 could be of interest as a new predictive factor of a favorable treatment response, and suggest new potential mechanisms of action of the therapeutic molecules. Whether such defect helps the progression of the disease from monoclonal gammopathy of unknown significance to MM remains, however, to be determined.

Indexed as

Bone MarrowDisease ProgressionFemaleGene ExpressionHumansImmunohistochemistryMaleMiddle AgedMultiple MyelomaProspective StudiesProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Real-Time Polymerase Chain ReactionRNA, MessengerSignal TransductionSTAT3 Transcription FactorProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6PTPN11 protein, humanPTPN6 protein, humanRNA, MessengerSOCS1 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorSuppressor of Cytokine Signaling 1 Protein

Identifiers

PMID28369102
PMCPMC5378363
OpenAlexW2604718785

What OpenQuestion holds

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LicenceCC BY
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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.