Evidence map›Paper›PMID 19560733›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2009

Molecular epidemiology of primary brain tumors.

Jun Gu, Yanhong Liu, Athanassios P Kyritsis, Melissa L Bondy

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 7 pooled it
3.9field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 7 syntheses or guidelines pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Association between the G870A polymorphism of Cyclin D1 gene and glioma risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  3. Assessment of the association between XRCC1 Arg399Gln polymorphism and glioma susceptibility.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  4. Association between XRCC3 Thr241Met polymorphism and risk of brain tumors: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  5. Pooled it
  6. Associations between three XRCC1 polymorphisms and glioma risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  7. Pooled it
  8. Trial
  9. Review
  10. Article
  11. Article
  12. Association of RNA mBioMed research international · 2023
    Article
  13. Article
  14. Role ofBiomedical reports · 2019
    Article
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  19. Article
  20. Nrf2 Expressions Correlate with WHO Grades in Gliomas and Meningiomas.International journal of molecular sciences · 2016
    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

4 authors at 2 institutions in 2 countries.

Jun GuSchool of Health Professions, University of Texas, M.D. Anderson Cancer Center, Houston, TX, 77030, USA.
Yanhong Liu
Athanassios P Kyritsis
Melissa L Bondy
The University of Texas MD Anderson Cancer Center · USUniversity Hospital of Ioannina · GR

Funding

Genetic Epidemiology of Glioma International ConsortiumR01CA119215 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BONDY, MELISSA L. · 2006 to 2010
$11.9M
MOLECULAR EPIDEMIOLOGY OF GLIOMASR01CA070917 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI BONDY, MELISSA L · 1996 to 2004
$3.0M
NCI NIH HHS 5R01 CA070917NCI NIH HHS 5R01 CA119215
6 · The paper itself

Abstract

Although primary brain tumors (PBTs) are generally considered to be a multifactorial disorder, understanding the genetic basis and etiology of the disease is essential for PBT risk assessment. Understanding of the genetic susceptibility for PBT has come from studies of rare genetic syndromes, linkage analysis, family aggregation, early-onset pediatric cases, and mutagen sensitivity. There are currently no effective markers to assess biological dose of exposures and genetic heterogeneity. The priorities recently recommended by the Brain Tumor Epidemiology Consortium emphasized the need for expanding research in genetics and molecular epidemiology. In this article, we review the literature to identify molecular epidemiologic case-control studies of PBTs that were hypothesis-driven and focused on four hypothesized candidate pathways: DNA repair, cell cycle, metabolism, and inflammation. We summarize the results in terms of genetic associations of single nucleotide polymorphisms of these pathways. We also discuss future research directions based on available evidence and technologies, and conclude that high resolution whole genome approach with significantly large sample size could rapidly advance our understanding of the genetic etiology of PBTs. Literature searches were done on PubMed in March 2009 with the terms glioma, glioblastoma, brain tumor, association, and polymorphism, and we only reviewed English language publications.

Indexed as

BiomarkersBrain NeoplasmsCell CycleDNA RepairGenetic Predisposition to DiseaseGenome-Wide Association StudyGliomaHumansMeningiomaMetabolismModels, BiologicalNeuroimmunomodulationPolymorphism, Single NucleotideBiomarkers

Identifiers

PMID19560733
PMCPMC5084179
OpenAlexW1964912639

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.