Evidence map›Paper›PMID 24358143›Full record

ArticlePloS one2013

Identification of novel genetic alterations in samples of malignant glioma patients.

Vedrana Milinkovic, Jasna Bankovic, Miodrag Rakic, Tijana Stankovic, Milica Skender-Gazibara, Sabera Ruzdijic, Nikola Tanic

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 26% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  20. Frequent loss of inositol polyphosphate-5-phosphatase in oropharyngeal squamous cell carcinoma.Journal of the European Academy of Dermatology and Venereology : JEADV · 2018
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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.

Vedrana MilinkovicUniversity of Belgrade, Institute for Biological Research "Sinisa Stankovic", Department of Neurobiology, Belgrade, Republic of Serbia.
Jasna BankovicUniversity of Belgrade, Institute for Biological Research "Sinisa Stankovic", Department of Neurobiology, Belgrade, Republic of Serbia.
Miodrag RakicClinical Center of Serbia, Clinic for Neurosurgery, Belgrade, Republic of Serbia.
Tijana StankovicUniversity of Belgrade, Institute for Biological Research "Sinisa Stankovic", Department of Neurobiology, Belgrade, Republic of Serbia.
Milica Skender-GazibaraUniversity of Belgrade, School of Medicine, Institute of Pathology, Belgrade, Republic of Serbia.
Sabera RuzdijicUniversity of Belgrade, Institute for Biological Research "Sinisa Stankovic", Department of Neurobiology, Belgrade, Republic of Serbia.
Nikola TanicUniversity of Belgrade, Institute for Biological Research "Sinisa Stankovic", Department of Neurobiology, Belgrade, Republic of Serbia.
University of Belgrade · RSCentar za Promociju Nauke · RSInstitute for Biological Research “Siniša Stanković”

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is the most frequent and malignant human brain tumor. High level of genomic instability detected in glioma cells implies that numerous genetic alterations accumulate during glioma pathogenesis. We investigated alterations in AP-PCR DNA profiles of 30 glioma patients, and detected specific changes in 11 genes not previously associated with this disease: LHFPL3, SGCG, HTR4, ITGB1, CPS1, PROS1, GP2, KCNG2, PDE4D, KIR3DL3, and INPP5A. Further correlations revealed that 8 genes might play important role in pathogenesis of glial tumors, while changes in GP2, KCNG2 and KIR3DL3 should be considered as passenger mutations, consequence of high level of genomic instability. Identified genes have a significant role in signal transduction or cell adhesion, which are important processes for cancer development and progression. According to our results, LHFPL3 might be characteristic of primary glioblastoma, SGCG, HTR4, ITGB1, CPS1, PROS1 and INPP5A were detected predominantly in anaplastic astrocytoma, suggesting their role in progression of secondary glioblastoma, while alterations of PDE4D seem to have important role in development of both glioblastoma subtypes. Some of the identified genes showed significant association with p53, p16, and EGFR, but there was no significant correlation between loss of PTEN and any of identified genes. In conclusion our study revealed genetic alterations that were not previously associated with glioma pathogenesis and could be potentially used as molecular markers of different glioblastoma subtypes.

Indexed as

Genomic InstabilityMutationAdultAgedAged, 80 and overAstrocytomaBrain NeoplasmsFemaleGlioblastomaHumansMaleMiddle AgedYoung Adult

Identifiers

PMID24358143
PMCPMC3864906
OpenAlexW2074483464

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.