Evidence map›Paper›PMID 26771524›Full record

ArticlePloS one2016

Expression and Polymorphism of Toll-Like Receptor 4 and Effect on NF-κB Mediated Inflammation in Colon Cancer Patients.

Abdelhabib Semlali, Narasimha Reddy Parine, Maha Arafah, Lamjed Mansour, Arezki Azzi, Omair Al Shahrani, Abdullah Al Amri, Jilani P Shaik, Abdulrahman M Aljebreen, Othman Alharbi and 5 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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

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  18. Phytochemical constituents and anticancer activities ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020
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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

15 authors at 5 institutions in 2 countries.

Abdelhabib SemlaliGenome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Narasimha Reddy ParineGenome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Maha ArafahCollege of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Lamjed MansourDepartment of Zoology, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Arezki AzziCollege of Medicine, Al Imam Muhammad Ibn Saud Islamic University (IMSIU), Riyadh, Kingdom of Saudi Arabia.
Omair Al ShahraniGenome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Abdullah Al AmriGenome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Jilani P ShaikGenome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Abdulrahman M AljebreenCollege of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Othman AlharbiCollege of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Majid A AlmadiDivision of Gastroenterology, King Khalid University Hospital, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Nahla Ali AzzamCollege of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Muhammad KohailanGenome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Mahmoud RouabhiaGroupe de Recherche en Écologie Buccale, Département de stomatologie, Faculté de Médecine Dentaire, Université Laval, Québec, Québec, Canada.
Mohammad Saud AlanaziGenome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia.
King Saud University · SAKing Khalid University Hospital · SAImam Mohammad ibn Saud Islamic University · SAMcGill University · CAUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our aim was to evaluate the association between the expression and the polymorphism of TLR4/NF-κB pathways and colon cancer. TLR4 (rs4986790, rs10759932, rs10759931 and rs2770150) were genotyped in blood samples from Colorectal patients and healthy controls. TLR4 and cytokines inflammatory expression were evaluated by real time PCR on 40 matching normal and colon tissues and the protein level by Immunohistochemistry. The high level of TLR4 expression in colon cancer tissues is mainly due to infections by bacteria in the human colon and leads to induction of an acute secretion of inflammatory cytokines mediated by NF-κB. Also, we report here a clear evidence for an association between TLR4 rs10759931 polymorphism (OR = 0.086, CI: 0.04-0.18, P = <0.00001). This polymorphism affects the entire population without being specific to either gender or to any age group. In contrast, the rs2770150 is associated with colon cancer in women aged over 50 years and is closely linked with the decreased levels of female sex hormones during the post-menopausal period (OR = 0.188, CI: 0.074-0.48, P = <0.00084). rs10759932 and rs4986790 appear to have any association with colon cancer. Our data suggest that TLR4 SNPs could possibly serve as biomarkers for decision making in colon cancer treatment.

Indexed as

Gene Expression Regulation, NeoplasticAgedAged, 80 and overColonic NeoplasmsFemaleHumansInflammationMaleMiddle AgedNF-kappa BPolymorphism, GeneticToll-Like Receptor 4NF-kappa BTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID26771524
PMCPMC4714746
OpenAlexW2243694148

What OpenQuestion holds

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LicenceCC BY
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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.