Evidence map›Paper›PMID 29282022›Full record

ArticleBMC cancer2017

Chromosomal instability induced by increased BIRC5/Survivin levels affects tumorigenicity of glioma cells.

Marina Conde, Susanne Michen, Ralf Wiedemuth, Barbara Klink, Evelin Schröck, Gabriele Schackert, Achim Temme

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Mechanotherapeutic Potential of Survivin in Glioblastoma.bioRxiv : the preprint server for biology · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
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  13. Article
  14. Article
  15. Natural Compounds as Promising Adjuvant Agents in The Treatment of Gliomas.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 3 institutions in 1 country.

Marina CondeDepartment of Neurosurgery, Section Experimental Neurosurgery/Tumor Immunology, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Susanne MichenDepartment of Neurosurgery, Section Experimental Neurosurgery/Tumor Immunology, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Ralf WiedemuthDepartment of Neurosurgery, Section Experimental Neurosurgery/Tumor Immunology, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Barbara KlinkInstitute for Clinical Genetics, Faculty of Medicine Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Evelin SchröckInstitute for Clinical Genetics, Faculty of Medicine Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Gabriele SchackertDepartment of Neurosurgery, Section Experimental Neurosurgery/Tumor Immunology, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Achim TemmeDepartment of Neurosurgery, Section Experimental Neurosurgery/Tumor Immunology, University Hospital Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Germany. achim.temme@uniklinikum-dresden.de.ORCID 0000-0001-5084-1180
German Cancer Research Center · DEUniversity Hospital Carl Gustav Carus · DENational Center for Tumor Diseases · DE

Funding

EU and Free State of Saxony EU-ESF GlioMath
6 · The paper itself

Abstract

backgroundSurvivin, belonging to the inhibitor of apoptosis (IAP) gene family, is abundantly expressed in tumors. It has been hypothesized that Survivin facilitates carcinogenesis by inhibition of apoptosis resulting in improved survival of tumorigenic progeny. Additionally, Survivin plays an essential role during mitosis. Together with its molecular partners Aurora B, Borealin and inner centromere protein it secures bipolar chromosome segregation. However, whether increased Survivin levels contribute to progression of tumors by inducing chromosomal instability remains unclear.

methodsWe overexpressed Survivin in U251-MG, SVGp12, U87-MG, HCT116 and p53-deficient U87-MG

resultsOverexpression of Survivin affected cells with knockdown of p53, cells harboring mutant p53 and SV40 large T antigen, respectively, resulting in the increase of cell fractions harboring 4n and >4n DNA contents. Increased γH2AX levels, indicative of DNA damage were monitored in all Survivin-transduced cell lines, but only in p53 wild type cells this was accompanied by an attenuated S-phase entry and activation of p21

conclusionsOur data suggest that increased Survivin levels promote adaptive evolution of tumors through combining induction of genetic heterogeneity with inhibition of apoptosis.

Indexed as

Chromosomal InstabilityAnimalsApoptosisCell ProliferationCell Transformation, NeoplasticDNA DamageGliomaHumansInhibitor of Apoptosis ProteinsMiceMice, NudeSurvivinTumor Cells, CulturedTumor Suppressor Protein p53Xenograft Model Antitumor AssaysBIRC5 protein, humanInhibitor of Apoptosis ProteinsSurvivinTP53 protein, humanTumor Suppressor Protein p53BIRC5/SurvivinChromosomal instabilityDNA damageGliomap53

Identifiers

PMID29282022
PMCPMC5745881
OpenAlexW2776712771

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.