Evidence map›Paper›PMID 10666371›Full record

ArticleThe American journal of pathology2000

Genetic profile of gliosarcomas.

R M Reis, D Könü-Lebleblicioglu, J M Lopes, P Kleihues, H Ohgaki

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing 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

99 citing papers in PubMed, 235 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. RAR-Dependent and RAR-Independent RXR Signaling in Stem-like Glioma Cells.International journal of molecular sciences · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

39 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

R M ReisInternational Agency for Research on Cancer, Lyon, France.
D Könü-Lebleblicioglu
J M Lopes
P Kleihues
H Ohgaki
Centre International de Recherche sur le Cancer · FRCommunauté urbaine de Lyon · FRUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There are distinct genetic pathways leading to the glioblastoma, the most malignant astrocytic brain tumor. Primary (de novo) glioblastomas develop in older patients and are characterized by epidermal growth factor (EGF) receptor amplification/overexpression, p16 deletion, and PTEN mutations, whereas secondary glioblastomas that progressed from low-grade or anaplastic astrocytoma develop in younger patients and frequently contain p53 mutations. In this study, we assessed the genetic profile of gliosarcoma, a rare glioblastoma variant characterized by a biphasic tissue pattern with alternating areas displaying glial and mesenchymal differentiation. Single-strand conformation polymorphism followed by direct DNA sequencing revealed p53 mutations in five of 19 gliosarcomas (26%) and PTEN mutations in seven cases (37%). Homozygous p16 deletion was detected by differential polymerase chain reaction in seven (37%) gliosarcomas. The overall incidence of alterations in the Rb pathway (p16 deletion, CDK4 amplification, or loss of pRb immunoreactivity) was 53%, and these changes were mutually exclusive. Coamplification of CDK4 and MDM2 was detected in one gliosarcoma. None of the gliosarcomas showed amplification or overexpression of the EGF receptor. Thus gliosarcomas exhibit a genetic profile similar to that of primary (de novo) glioblastomas, except for the absence of EGFR amplification/overexpression. Identical PTEN mutations in the gliomatous and sarcomatous tumor components were found in two cases. Other biopsies contained p16 deletions, an identical p53 mutation, or coamplification of MDM2 and CDK4 in both tumor areas. This strongly supports the concept of a monoclonal origin of gliosarcomas and an evolution of the sarcomatous component due to aberrant mesenchymal differentiation in a highly malignant astrocytic neoplasm.

Indexed as

Nuclear ProteinsTumor Suppressor ProteinsAdultAgedCyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent KinasesErbB ReceptorsFemaleGene AmplificationGene DeletionGene ExpressionGliosarcomaHumansMaleMiddle AgedCDK4 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent KinasesErbB ReceptorsMDM2 protein, humanNuclear ProteinsPhosphoric Monoester HydrolasesProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Proto-Oncogene Proteins c-metPTEN PhosphohydrolasePTEN protein, humanRetinoblastoma ProteinTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID10666371
PMCPMC1850048
OpenAlexW2155870124

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.