Evidence map›Paper›PMID 27992526›Full record

ArticlePloS one2016

3'UTR Polymorphism in ACSL1 Gene Correlates with Expression Levels and Poor Clinical Outcome in Colon Cancer Patients.

Teodoro Vargas, Juan Moreno-Rubio, Jesús Herranz, Paloma Cejas, Susana Molina, Marta Mendiola, Emilio Burgos, Ana B Custodio, María De Miguel, Roberto Martín-Hernández and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. The Association ofBalkan journal of medical genetics : BJMG · 2025
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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

13 authors at 3 institutions in 2 countries.

Teodoro VargasMolecular Oncology, IMDEA-Food Institute, CEI UAM+CSIC, Madrid, Spain.
Juan Moreno-RubioMolecular Oncology, IMDEA-Food Institute, CEI UAM+CSIC, Madrid, Spain.
Jesús HerranzBiostatistics and Bioinformatics Unit, IMDEA-Food Institute, CEI UAM+CSIC, Madrid, Spain.
Paloma CejasTranslational Oncology Laboratory, La Paz University Hospital (IdiPAZ), Madrid, Spain.
Susana MolinaMolecular Oncology, IMDEA-Food Institute, CEI UAM+CSIC, Madrid, Spain.
Marta MendiolaTranslational Oncology Laboratory, La Paz University Hospital (IdiPAZ), Madrid, Spain.
Emilio BurgosPathology Department, La Paz University Hospital (IdiPAZ), Madrid, Spain.
Ana B CustodioMedical Oncology, La Paz University Hospital (IdiPAZ), Madrid, Spain.
María De MiguelTranslational Oncology Laboratory, La Paz University Hospital (IdiPAZ), Madrid, Spain.
Roberto Martín-HernándezBiostatistics and Bioinformatics Unit, IMDEA-Food Institute, CEI UAM+CSIC, Madrid, Spain.
Guillermo RegleroMolecular Oncology, IMDEA-Food Institute, CEI UAM+CSIC, Madrid, Spain.
Jaime FeliuMedical Oncology, La Paz University Hospital (IdiPAZ), Madrid, Spain.
Ana Ramírez de MolinaMolecular Oncology, IMDEA-Food Institute, CEI UAM+CSIC, Madrid, Spain.
Hospital Universitario La Paz · ESMadrid Institute for Advanced Studies · ESIMDEA Food · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Strong evidence suggests that lipid metabolism (LM) has an essential role in tumor growth to support special energetic and structural requirements of tumor cells. Recently, overexpression of LM-related genes, apolipoproteins related to metabolic syndrome, and ACSL/SCD network involved in fatty acid activation have been proposed as prognostic markers of colon cancer (CC). Furthermore, activation of this latter lipid network has been recently demonstrated to confer invasive and stem cell properties to tumor cells promoting tumor aggressiveness and patient relapse. With the aim of elucidating whether any genetic variation within these genes could influence basal expression levels and consequent susceptibility to relapse, we genotype, in 284 CC patients, 57 polymorphisms located in the 7 genes of these lipid networks previously associated with worse clinical outcome of CC patients (ABCA1, ACSL1, AGPAT1, APOA2, APOC1, APOC2 and SCD), some of them related to CC aggressiveness. After adjusting with clinical confounding factors and multiple comparisons, an association between genotype and disease-free survival (DFS) was shown for rs8086 in 3'-UTR of ACSL1 gene (HR 3.08; 95% CI 1.69-5.63; adjusted p = 0.046). Furthermore, the risk T/T genotype had significantly higher ACSL1 gene expression levels than patients carrying C/T or C/C genotype (means = 5.34; 3.73; 2.37 respectively; p-value (ANOVA) = 0.019), suggesting a functional role of this variant. Thus, we have identified a "risk genotype" of ACSL1 gene that confers constitutive high levels of the enzyme, which is involved in the activation of fatty acids through conversion to acyl-CoA and has been recently related to increased invasiveness of tumor cells. These results suggest that rs8086 of ACSL1 could be a promising prognostic marker in CC patients, reinforcing the relevance of LM in the progression of CC.

Indexed as

3' Untranslated RegionsPolymorphism, Single NucleotideAdultAgedAged, 80 and overCoenzyme A LigasesColonic NeoplasmsDisease-Free SurvivalFemaleGene FrequencyGenetic Predisposition to DiseaseHumansMaleMiddle AgedPrognosisRetrospective Studies3' Untranslated RegionsACSL1 protein, humanCoenzyme A Ligases

Identifiers

PMID27992526
PMCPMC5167383
OpenAlexW2562364750

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.