Evidence map›Paper›PMID 22294764›Full record

ArticleMutagenesis2012

Genetic polymorphisms in fatty acid metabolism genes and colorectal cancer.

M Crous-Bou, G Rennert, R Salazar, F Rodriguez-Moranta, H S Rennert, F Lejbkowicz, L Kopelovich, S M Lipkin, S B Gruber, V Moreno

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Mutagenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 4 pooled it
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 4 syntheses or guidelines pooled it, 48 citations in OpenAlex.

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  3. Effect of Proliferator-Activated Receptor-γ Pro12Ala Polymorphism on Colorectal Cancer Risk: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015
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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

10 authors at 9 institutions in 3 countries.

M Crous-BouColorectal Cancer Group, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona 08907, Spain.
G Rennert
R Salazar
F Rodriguez-Moranta
H S Rennert
F Lejbkowicz
L Kopelovich
S M Lipkin
S B Gruber
V Moreno
Institut d'Investigació Biomédica de Bellvitge · ESCarmel Medical Center · ILClalit Health Services · ILCornell University · USInstitut Català d'Oncologia · ESNational Cancer Institute · USTechnion – Israel Institute of Technology · ILUniversitat de Barcelona · ESUniversity of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
Transdisciplinary Studies of Genetic Variation in Colorectal CancerU19CA148107 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GRUBER, STEPHEN B · 2010 to 2014
$11.1M
MOLECULAR EPIDEMIOLOGY OF COLORECTAL CANCERR01CA081488 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GRUBER, STEPHEN B · 1999 to 2008
$9.2M
NCI NIH HHS 5 P30 CA46592NCI NIH HHS N01-CN43308NCI NIH HHS NCI R01-CA81488NCI NIH HHS U19 CA148107
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a leading cause of cancer death worldwide. Epidemiological risk factors for CRC included dietary fat intake; consequently, the role of genes in the fatty acid biosynthesis and metabolism pathways is of particular interest. Moreover, hyperlipidaemia has been associated with different type of cancer and serum lipid levels could be affected by genetic factors, including polymorphisms in the lipid metabolism pathway. The aim of this study is to assess the association between single-nucleotide polymorphisms (SNPs) in fatty acid metabolism genes, serum lipid levels, body mass index (BMI) and dietary fat intake and CRC risk; 30 SNPs from 8 candidate genes included in fatty acid biosynthesis and metabolism pathways were genotyped in 1780 CRC cases and 1864 matched controls from the Molecular Epidemiology of Colorectal Cancer study. Information on clinicopathological characteristics, lifestyle and dietary habits were also obtained. Logistic regression and association analysis were conducted. Several LIPC (lipase, hepatic) polymorphisms were found to be associated with CRC risk, although no particular haplotype was related to CRC. The SNP rs12299484 showed an association with CRC risk after Bonferroni correction. We replicate the association between the T allele of the LIPC SNP rs1800588 and higher serum high-density lipoprotein levels. Weak associations between selected polymorphism in the LIPC and PPARG genes and BMI were observed. A path analysis based on structural equation modelling showed a direct effect of LIPC gene polymorphisms on colorectal carcinogenesis as well as an indirect effect mediated through serum lipid levels. Genetic polymorphisms in the hepatic lipase gene have a potential role in colorectal carcinogenesis, perhaps though the regulation of serum lipid levels.

Indexed as

Genetic Predisposition to DiseaseAgedBody Mass IndexCase-Control StudiesColorectal NeoplasmsFatty AcidsFemaleHaplotypesHumansIsraelLipaseMaleNeoplasm ProteinsPolymorphism, Single NucleotideRisk FactorsFatty AcidsLipaseNeoplasm Proteins

Identifiers

PMID22294764
PMCPMC3269001
OpenAlexW2118653540

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.