Evidence map›Paper›PMID 27197070›Full record

ArticleThe Prostate2016

Impact of Genetic and Epigenetic Variations Within the FADS Cluster on the Composition and Metabolism of Polyunsaturated Fatty Acids in Prostate Cancer.

Tao Cui, Austin G Hester, Michael C Seeds, Elaheh Rahbar, Timothy D Howard, Susan Sergeant, Floyd H Chilton

Open access · hybridAbstract read
In one paragraph

Article in The Prostate, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Frontiers in nutrition · 2026
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  17. Allele-specific methylation in theClinical epigenetics · 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 1 institution in 1 country.

Tao CuiDepartment of Urology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Austin G HesterDepartment of Urology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Michael C SeedsDepartment of Internal Medicine, Section on Translational and Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Elaheh RahbarDepartment of Biomedical Engineering, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Timothy D HowardDepartment of Internal Medicine, Section on Genetics and Genomics, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Susan SergeantDepartment of Biochemistry, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Floyd H ChiltonDepartment of Physiology and Pharmacology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Wake Forest University · US

Funding

The Wake Forest Center for Botanical Lipids and Inflammatory Disease PreventionP50AT002782 · NCCIH · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHILTON, FLOYD H · 2005 to 2014
$15.3M
NCCIH NIH HHS P50 AT002782
6 · The paper itself

Abstract

backgroundIn vitro and experimental animal studies have demonstrated that high levels of omega-6 (n-6) polyunsaturated fatty acids (PUFAs) and high ratios of n-6 to omega-3 (n-3) PUFAs are strongly associated with the development and progression of prostate cancer (PCA). However, epidemiological studies in humans have demonstrated inconsistent findings linking dietary PUFAs and PCA risk. We hypothesize that genetic and epigenetic variations within the fatty acid desaturase (FADS) gene cluster produce gene-diet interactions that may explain these disparate findings. This study tested the relationship of the genotype of a single nucleotide polymorphism, rs174537, and the methylation status of a CpG site, cg27386326, with PUFA composition, and markers of PUFA biosynthesis in PCA tissue.

methodsSixty PCA specimens from patients undergoing radical prostatectomy were genotyped, pyrosequenced and quantitated for fatty acids (FAs).

resultsLong-chain (LC)-PUFAs, such as arachidonic acid (ARA), were abundant in these specimens, with ARA accounting for 15.8% of total FAs. In addition, there was a positive association of the G allele at rs174537 with concentrations of ARA and adrenic acid and ratios of products to precursors within the n-6 PUFA pathway such that specimens from homozygous G individuals exhibited increasingly higher values as compared to specimens from heterozygous individuals and homozygous T individuals. Finally, the methylation status of cg27386326 was inversely correlated with tissue concentrations of LC-PUFAs and markers of LC-PUFA biosynthesis.

conclusionsThese data reveal that genetic and epigenetic variations within the FADS cluster are highly associated with LC-PUFA concentrations and LC-PUFA biosynthetic capacity in PCA tissue. They also raise the potential that gene-PUFA interactions play an important role in PCA risk and severity. Prostate 76:1182-1191, 2016. © 2016 The Authors. The Prostate published by Wiley Periodicals, Inc.

Indexed as

AgedAnimalsEpigenesis, GeneticFatty Acid DesaturasesFatty Acids, UnsaturatedGenetic VariationHumansMaleMiddle AgedMultigene FamilyProstatic NeoplasmsFatty Acid DesaturasesFatty Acids, Unsaturatedarachidonic acidcg27386326omega-6PUFArs174537

Identifiers

PMID27197070
PMCPMC6680327
OpenAlexW2407855874

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.