Evidence map›Paper›PMID 12080466›Full record

ArticleOncogene2002

The tumor suppressor activity of SOCS-1.

Robert Rottapel, Subburaj Ilangumaran, Christopher Neale, Jose La Rose, Jenny M-Y Ho, Melody H-H Nguyen, Dwayne Barber, Patrice Dubreuil, Paulo de Sepulveda

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. SOCS proteins in regulation of receptor tyrosine kinase signaling.Cellular and molecular life sciences : CMLS · 2014
    Review
  14. Review
  15. Suppression of cytokine signaling: the SOCS perspective.Cytokine & growth factor reviews · 2013
    Review
  16. Article
  17. Targetome profiling, pathway analysis and genetic association study implicate miR-202 in lymphomagenesis.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2013
    Article
  18. Suppressor of cytokine signaling 1 blocks mitosis in human melanoma cells.Cellular and molecular life sciences : CMLS · 2013
    Article
  19. Article
  20. SOCS proteins in development and disease.American journal of clinical and experimental immunology · 2013
    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 3 institutions in 2 countries.

Robert RottapelDepartment of Immunology, University of Toronto, Canada. rottapel@oci.utoronto.ca
Subburaj Ilangumaran
Christopher Neale
Jose La Rose
Jenny M-Y Ho
Melody H-H Nguyen
Dwayne Barber
Patrice Dubreuil
Paulo de Sepulveda
Ontario Institute for Cancer Research · CAUniversity of Toronto · CAInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SOCS-1 is an inducible SH2-containing inhibitor of Jak kinases and as such can potently suppress cytokine signaling. SOCS-1 deficient mice die within the first three weeks of life from a myeloproliferative disorder driven by excessive interferon signaling. We report here that SOCS-1 inhibits proliferation signals induced by a variety of oncogenes active within the hematopoietic system. Ectopic expression of SOCS-1 abolished proliferation mediated by a constitutively active form of the KIT receptor, TEL-JAK2, and v-ABL, and reduced metastasis from BCR-ABL transformed cells. SOCS-1, however, did not interfere with v-SRC or RASV12 mediated cellular transformation. A mutant form of SOCS-1 unable to bind through its SH2 domain to tyrosine phosphorylated proteins could still inhibit KIT, but not TEL-JAK2, indicating multiple mechanisms for SOCS-1-mediated tumor suppression. We show that the steady state levels of TEL-JAK2 and to a greater extent v-ABL are diminished in the presence of SOCS-1. Lastly, we show that SOCS-1 -/- fibroblasts are more sensitive than wild type fibroblasts to either spontaneous or oncogene-induced transformation. These data suggest that loss-of-function of SOCS-1 may collaborate with a variety of hematopoietic oncogenes to facilitate tumor progression.

Indexed as

Proto-Oncogene ProteinsAnimalsCarrier ProteinsCell DivisionCell Transformation, NeoplasticDNA-Binding ProteinsETS Translocation Variant 6 ProteinFibroblastsFusion Proteins, bcr-ablGenes, Tumor SuppressorHematopoietic Stem CellsJanus Kinase 2MiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein KinasesCarrier ProteinsDNA-Binding ProteinsETS Translocation Variant 6 ProteinFusion Proteins, bcr-ablJAK2 protein, humanJak2 protein, mouseJanus Kinase 2Mitogen-Activated Protein KinasesOncogene Proteins, FusionOncogene Proteins v-ablp38 Mitogen-Activated Protein KinasesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-kitRepressor ProteinsSocs1 protein, mouseStat1 protein, mouseSTAT1 Transcription FactorSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTEL-JAK2 fusion protein, humanTEL-JAK2 fusion protein, mouseTrans-Activators

Identifiers

PMID12080466
OpenAlexW2322599576

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.