Evidence map›Paper›PMID 15116098›Full record

ArticleOncogene2004

Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene.

Christina EL Naaman, Birgitte Grum-Schwensen, Ahmed Mansouri, Mariam Grigorian, Eric Santoni-Rugiu, Thomas Hansen, Marina Kriajevska, Beat W Schafer, Claus W Heizmann, Eugene Lukanidin and 1 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Review
  3. S100 proteins in obesity: liaisons dangereuses.Cellular and molecular life sciences : CMLS · 2020
    Review
  4. Article
  5. Yonsei medical journal · 2018
    Article
  6. Article
  7. S100A4 protects the myocardium against ischemic stress.Journal of molecular and cellular cardiology · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. S100A4 in esophageal cancer: is this the one to blame?World journal of gastroenterology · 2012
    Article
  17. Article
  18. Article
  19. Article
  20. S100A4 and metastasis: a small actor playing many roles.The American journal of pathology · 2010
    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

11 authors at 4 institutions in 3 countries.

Christina EL NaamanDepartment of Molecular Cancer Biology, Danish Cancer Society, Strandboulevarden 49, DK2100 Copenhagen, Denmark.
Birgitte Grum-Schwensen
Ahmed Mansouri
Mariam Grigorian
Eric Santoni-Rugiu
Thomas Hansen
Marina Kriajevska
Beat W Schafer
Claus W Heizmann
Eugene Lukanidin
Noona Ambartsumian
Danish Cancer Society · DKUniversity of Zurich · CHMax Planck Institute for Biophysical Chemistry · DERigshospitalet · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis-promoting Mts1(S100A4) protein belongs to the S100 family of Ca(2+)-binding proteins. A mouse strain with a germ-line inactivation of the S100A4 gene was generated. The mice were viable and did not display developmental abnormalities in the postnatal period. However, an abnormal sex ratio was observed in the litters with the S100A4-/- genotype, raising the possibility of a certain level of embryonic lethality in this strain. In all, 10% of 10-14-month-old S100A4-null animals developed tumors. This is a characteristic feature of mouse strains with inactivated tumor suppressor genes. Spontaneous tumors of S100A4-/- mice were p53 positive. Recently, we have shown that S100A4 interacts with p53 tumor suppressor protein and induces apoptosis. We proposed that impairment of this interaction could affect the apoptosis-promoting function of p53 that is involved in its tumor suppressor activity. The frequency of apoptosis in the spleen of S100A4-/- animals after whole-body gamma-irradiation was reduced compared to the wild-type animals. The same was true for the transcriptional activation of the p53 target genes - waf/p21/cip1 and bax. Taken together, these observations indicate that spontaneous tumors in S100A4-/- mice are a result of functional destabilization of p53 tumor suppressor gene.

Indexed as

Genetic Predisposition to DiseaseProto-Oncogene Proteins c-bcl-2Animalsbcl-2-Associated X ProteinCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsGamma RaysMiceNeoplasm MetastasisNeoplasmsProto-Oncogene ProteinsSpleenThymus GlandTumor Suppressor Protein p53Bax protein, mousebcl-2-Associated X ProteinCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Tumor Suppressor Protein p53

Identifiers

PMID15116098
OpenAlexW2156872018

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.