Evidence map›Paper›PMID 27807069›Full record

ArticleCancer genomics & proteomics

A Comparative Study of the Molecular Characteristics of Familial Gliomas and Other Cancers.

Jie Lu, Mark G Burnett, Max Shpak

Abstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Up-Regulation ofCell journal · 2021
    Article
  3. Review
  4. 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

3 authors.

Jie LuNeuroTexas Institute Research Foundation, St. David's Medical Center, Austin, Texas, TX, U.S.A.
Mark G BurnettNeuroTexas Institute Research Foundation, St. David's Medical Center, Austin, Texas, TX, U.S.A.
Max ShpakNeuroTexas Institute Research Foundation, St. David's Medical Center, Austin, Texas, TX, U.S.A. shpak.max@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFamilial cancers are those that co-occur among first-degree relatives without showing Mendelian patterns of inheritance. MATERIALS AND

methodsIn this analysis, we compare the genomic characteristics of familial and sporadic cancers, with a focus on low-grade gliomas (LGGs) using sequence and expression data from the Cancer Genome Atlas.

resultsFamilial cancers show similar genomic and molecular biomarker profiles to sporadic cancers, consistent with the similarity in their clinical features. There are no statistically significant differences among somatic mutation, copy number variant, or gene expression patterns between familial and sporadic cancers; methylation profiles are the only class of molecular data to show significant differences.

conclusionFamilial cancers are likely driven by multiple, individually weak contributions to familiality (i.e. large numbers of alleles and/or shared environmental risks). Consequently, these risk factors tend to be obscured by stronger confounding variables such as clinical or molecular variation among cancer subtypes.

Indexed as

AllelesBiomarkers, TumorDNA Copy Number VariationsGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGerm-Line MutationGliomaHumansNeoplasm GradingNeoplasm ProteinsRisk FactorsBiomarkers, TumorNeoplasm Proteinscancer risk allelesFamilial cancergene expressiongene methylationlow-grade glioma

Identifiers

PMID27807069
PMCPMC5219920

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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.