Evidence map›Paper›PMID 20212223›Full record

ReviewArchives of neurology2010

New insights into susceptibility to glioma.

Yanhong Liu, Sanjay Shete, Fay J Hosking, Lindsay B Robertson, Melissa L Bondy, Richard S Houlston

Open access · bronzeAbstract readReview
In one paragraph

Review in Archives of neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Implications of risk conferred by 5p15.33 loci genetic variants; human telomerase reverse transcriptase rs2736098 and rs2736100 in predisposition of bladder cancer.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2022
    Article
  6. Review
  7. Article
  8. Genetic Modulation of Neurocognitive Function in Glioma Patients.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    Article
  9. Genetic variants in N-myc (and STAT) interactor and susceptibility to glioma in a Chinese Han population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  10. The CDKN2A-CDKN2B rs4977756 polymorphism and glioma risk: a meta-analysis.International journal of clinical and experimental medicine · 2015
    Article
  11. Article
  12. Neuro-oncology: Five new things.Neurology. Clinical practice · 2013
    Article
  13. Article
  14. Article
  15. 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

6 authors at 1 institution in 1 country.

Yanhong LiuDepartment of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Unit 1340, PO Box 301439, Houston, TX 77230-1439, USA.
Sanjay Shete
Fay J Hosking
Lindsay B Robertson
Melissa L Bondy
Richard S Houlston
Cancer Genetics (United States) · US

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 5R01CA070917NCI NIH HHS 5R01CA119215NCI NIH HHS R01 CA070917NCI NIH HHS R01 CA119215Wellcome Trust
6 · The paper itself

Abstract

The study of inherited susceptibility to cancer has been one of the most informative areas of research in the past decade. Most of the cancer genetics studies have been focused on the common tumors such as breast and colorectal cancers. As the allelic architecture of these tumors is unraveled, research attention is turning to other rare cancers such as glioma, which are also likely to have a major genetic component as the basis of their development. In this brief review we discuss emerging data on glioma whole genome-association searches to identify risk loci. Two glioma genome-wide association studies have so far been reported. Our group identified 5 risk loci for glioma susceptibility (TERT rs2736100, CCDC26 rs4295627, CDKN2A/CDKN2B rs4977756, RTEL1 rs6010620, and PHLDB1 rs498872). Wrensch and colleagues provided further evidence to 2 risk loci (CDKN2B rs1412829 and RTEL1 rs6010620) for GBM and anaplastic astrocytoma. Although these data provide the strongest evidence to date for the role of common low-risk variants in the etiology of glioma, the single-nucleotide polymorphisms identified alone are unlikely to be candidates for causality. Identifying the causal variant at each specific locus and its biological impact now poses a significant challenge, contingent on a combination of fine mapping and functional analyses. Finally, we hope that a greater understanding of the biological basis of the disease will lead to the development of novel therapeutic interventions.

Indexed as

AllelesCentral Nervous System NeoplasmsGenetic Predisposition to DiseaseGenetic VariationGliomaHumans

Identifiers

PMID20212223
PMCPMC5929984
OpenAlexW1999216984

What OpenQuestion holds

Textmetadata
LicenceTDM
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.