Evidence map›Paper›PMID 18981259›Full record

ArticleNeuro-oncology2009

Pediatric glioblastomas: a histopathological and molecular genetic study.

Vaishali Suri, Prasenjit Das, Pankaj Pathak, Ayushi Jain, Mehar Chand Sharma, Sachin Anil Borkar, Ashish Suri, Deepak Gupta, Chitra Sarkar

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.2field-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

56 citing papers in PubMed, 106 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Asian journal of neurosurgery · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. H3K27M, IDH1, and ATRX expression in pediatric GBM and their clinical and prognostic significance.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2019
    Article
  15. The Extracellular Matrix and Biocompatible Materials in Glioblastoma Treatment.Frontiers in bioengineering and biotechnology · 2019
    Review
  16. FNA Cytology in pediatric small cell glioblastoma.Acta bio-medica : Atenei Parmensis · 2018
    Article
  17. Article
  18. Extent of surgical resection and adjuvant temozolomide improves survival in pediatric GBM: a single center experience.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2017
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Vaishali SuriDepartment of Pathology, All India Institute of Medical Sciences, New Delhi-110029, India.
Prasenjit Das
Pankaj Pathak
Ayushi Jain
Mehar Chand Sharma
Sachin Anil Borkar
Ashish Suri
Deepak Gupta
Chitra Sarkar
All India Institute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) occurs rarely in children. Relatively few studies have been performed on molecular properties of pediatric GBMs. Our objective in this study was to evaluate the genetic alterations in pediatric GBM (age < or = 18 years) with special reference to p53, p16, and p27 protein expression, alterations of the epidermal growth factor receptor (EGFR), and deletion of the phosphate and tensin homolog gene (PTEN). Thirty cases of childhood GBMs reported between January 2002 and June 2007 were selected, and slides stained with hematoxylin and eosin were reviewed. Immunohistochemical staining was performed for EGFR, p53, p16, and p27, and tumor proliferation was assessed by calculating the MIB-1 labeling index (LI). Fluorescence in situ hybridization analysis was performed to evaluate for EGFR amplification and PTEN deletion. Histopathological features and MIB-1 LI were similar to adult GBMs. p53 protein expression was observed in 63%. Although EGFR protein overexpression was noted in 23% of cases, corresponding amplification of the EGFR gene was rare (5.5%). Deletion of the PTEN gene was also equally rare (5.5%). One case showed polysomy (chromosomal gains) of chromosomes 7 and 10. Loss of p16 and p27 immunoexpression was observed in 68% and 54% of cases, respectively. In pediatric de novo/primary GBMs, deletion of PTEN and EGFR amplification are rare, while p53 alterations are more frequent compared to primary adult GBMs. Frequency of loss of p16 and p27 immunoexpression is similar to their adult counterparts. This suggests that pediatric malignant gliomas are distinctly different from adult GBMs, highlighting the need for identification of molecular targets that may be adopted for future novel therapeutic strategies.

Indexed as

AdolescentBrain NeoplasmsChildChild, PreschoolCyclin-Dependent Kinase Inhibitor p16ErbB ReceptorsFemaleGene ExpressionGlioblastomaHumansImmunohistochemistryInfantIn Situ Hybridization, FluorescenceKi-67 AntigenMaleProliferating Cell Nuclear AntigenCyclin-Dependent Kinase Inhibitor p16ErbB ReceptorsKi-67 Antigenp27 antigenProliferating Cell Nuclear AntigenPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Protein p53

Identifiers

PMID18981259
PMCPMC2718971
OpenAlexW2096298496

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.