Evidence map›Paper›PMID 29040662›Full record

ArticleNeuro-oncology2018

Molecular subtyping of tumors from patients with familial glioma.

Vanessa Y Ruiz, Corinne E Praska, Georgina Armstrong, Thomas M Kollmeyer, Seiji Yamada, Paul A Decker, Matthew L Kosel, Jeanette E Eckel-Passow, Daniel H Lachance, Matthew N Bainbridge and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in oncology · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. 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

14 authors at 5 institutions in 2 countries.

Vanessa Y RuizDepartment of Laboratory Medicine and Pathology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Rochester, Minnesota, USA.
Corinne E PraskaDepartment of Laboratory Medicine and Pathology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Rochester, Minnesota, USA.
Georgina ArmstrongDepartment of Medicine, Section of Epidemiology and Population Sciences, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA.
Thomas M KollmeyerDepartment of Laboratory Medicine and Pathology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Rochester, Minnesota, USA.
Seiji YamadaDepartment of Laboratory Medicine and Pathology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Rochester, Minnesota, USA.
Paul A DeckerDivision of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Matthew L KoselDivision of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Jeanette E Eckel-PassowDivision of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Daniel H LachanceDepartment of Neurology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Rochester, Minnesota, USA.
Matthew N BainbridgeRady Children's Institute for Genomic Medicine, Rady Children's Hospital, San Diego, California, USA.
Beatrice S MelinDepartment of Radiation Sciences, Faculty of Medicine, Umea° University, Umeå, Sweden.
Melissa L BondyDepartment of Medicine, Section of Epidemiology and Population Sciences, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA.
Robert B JenkinsDepartment of Laboratory Medicine and Pathology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Rochester, Minnesota, USA.
Gliogene Consortium
Mayo Clinic · USWinnMed · USBaylor College of Medicine · USRady Children's Hospital-San Diego · USUmeå University · SE

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Targeted MV-CEA as a Potent Antitumor Agent against GBMP50CA108961 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2004 to 2015
$22.5M
GENETIC EPIDEMIOLOGY OF MALIGNANT GLIOMAR01CA052689 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WIENCKE, JOHN K., WRENSCH, MARGARET R. · 1991 to 2015
$20.5M
International Case Control Study of Malignant GliomaR01CA139020 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BONDY, MELISSA L. · 2010 to 2015
$16.0M
TRAINING IN TRANSLATIONAL RESEARCH: BENCH TO BEDSIDER25GM055252 · NIGMS · MAYO CLINIC ROCHESTER · PI LUJAN, LUIS, MAHER, LOUIS JAMES · 1996 to 2022
$8.3M
Post-baccalaureate Training in Biomedical ResearchR25GM075148 · NIGMS · MAYO CLINIC ROCHESTER · PI LUJAN, LUIS, MAHER, LOUIS JAMES · 2006 to 2024
$6.1M
Identification of 9p and 20q Germline Alterations in Glioblastoma PathogenesisRC1NS068222 · NINDS · MAYO CLINIC ROCHESTER · PI JENKINS, ROBERT B. · 2009 to 2010
$984k
NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA108961NCI NIH HHS R01 CA052689NCI NIH HHS R01 CA139020NIGMS NIH HHS R25 GM055252NIGMS NIH HHS R25 GM075148NIH HHS P50CA108961NIH HHS R01CA139020NIH HHS R01CA52689NIH HHS R25GM075148NIH HHS RC1NS068222ZNINDS NIH HHS RC1 NS068222
6 · The paper itself

Abstract

Background: Single-gene mutation syndromes account for some familial glioma (FG); however, they make up only a small fraction of glioma families. Gliomas can be classified into 3 major molecular subtypes based on isocitrate dehydrogenase (IDH) mutation and 1p/19q codeletion. We hypothesized that the prevalence of molecular subtypes might differ in familial versus sporadic gliomas and that tumors in the same family should have the same molecular subtype. Methods: Participants in the FG study (Gliogene) provided samples for germline DNA analysis. Formalin-fixed, paraffin-embedded tumors were obtained from a subset of FG cases, and DNA was extracted. We analyzed tissue from 75 families, including 10 families containing a second affected family member. Copy number variation data were obtained using a first-generation Affymetrix molecular inversion probe (MIP) array. Results: Samples from 62 of 75 (83%) FG cases could be classified into the 3 subtypes. The prevalence of the molecular subtypes was: 30 (48%) IDH-wildtype, 21 (34%) IDH-mutant non-codeleted, and 11 (19%) IDH-mutant and 1p/19q codeleted. This distribution of molecular subtypes was not statistically different from that of sporadic gliomas (P = 0.54). Of 10 paired FG samples, molecular subtypes were concordant for 7 (κ = 0.59): 3 IDH-mutant non-codeleted, 2 IDH-wildtype, and 2 IDH-mutant and 1p/19q codeleted gliomas. Conclusions: Our data suggest that within individual families, patients develop gliomas of the same molecular subtype. However, we did not observe differences in the prevalence of the molecular subtypes in FG compared with sporadic gliomas. These observations provide further insight into the distribution of molecular subtypes in FG.

Indexed as

DNA Copy Number VariationsGenetic Predisposition to DiseaseMutationBrain NeoplasmsChromosome AberrationsFemaleGliomaHumansIsocitrate DehydrogenaseMaleMiddle AgedNeoplasm GradingPedigreePrognosisIDH1 protein, humanIDH2 protein, humanIsocitrate Dehydrogenase

Identifiers

PMID29040662
PMCPMC5961123
OpenAlexW2763895507

What OpenQuestion holds

Textmetadata
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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.