Evidence map›Paper›PMID 29455641›Full record

SynthesisBMC medicine2018

Circadian pathway genetic variation and cancer risk: evidence from genome-wide association studies.

Simone Mocellin, Saveria Tropea, Clara Benna, Carlo Riccardo Rossi

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in BMC medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 109 citations in OpenAlex.

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  18. Circadian rhythm disruption and endocrine-related tumors.World journal of clinical oncology · 2024
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2 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Simone MocellinDepartment of Surgery Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128, Padova, Italy. simone.mocellin@unipd.it.ORCID 0000-0002-9433-8445
Saveria TropeaIstituto Oncologico Veneto, IOV-IRCCS, Padova, Italy.
Clara BennaDepartment of Surgery Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128, Padova, Italy.
Carlo Riccardo RossiDepartment of Surgery Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128, Padova, Italy.
University of Padua · ITIstituto Oncologico Veneto · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDysfunction of the circadian clock and single polymorphisms of some circadian genes have been linked to cancer susceptibility, although data are scarce and findings inconsistent. We aimed to investigate the association between circadian pathway genetic variation and risk of developing common cancers based on the findings of genome-wide association studies (GWASs).

methodsSingle nucleotide polymorphisms (SNPs) of 17 circadian genes reported by three GWAS meta-analyses dedicated to breast (Discovery, Biology, and Risk of Inherited Variants in Breast Cancer (DRIVE) Consortium; cases, n = 15,748; controls, n = 18,084), prostate (Elucidating Loci Involved in Prostate Cancer Susceptibility (ELLIPSE) Consortium; cases, n = 14,160; controls, n = 12,724) and lung carcinoma (Transdisciplinary Research In Cancer of the Lung (TRICL) Consortium; cases, n = 12,160; controls, n = 16,838) in patients of European ancestry were utilized to perform pathway analysis by means of the adaptive rank truncated product (ARTP) method. Data were also available for the following subgroups: estrogen receptor negative breast cancer, aggressive prostate cancer, squamous lung carcinoma and lung adenocarcinoma.

resultsWe found a highly significant statistical association between circadian pathway genetic variation and the risk of breast (pathway P value = 1.9 × 10

conclusionsOur findings, based on the largest series ever utilized for ARTP-based gene and pathway analysis, support the hypothesis that circadian pathway genetic variation is involved in cancer predisposition.

Indexed as

Circadian ClocksGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansNeoplasmsPolymorphism, Single NucleotideRiskCancer predispositionCancer riskCircadian clockGene pathwayGenetic variationGenome-wide association study (GWAS)GermlinePathway analysisSingle nucleotide polymorphism (SNP)

Identifiers

PMID29455641
PMCPMC5817863
OpenAlexW2788669874

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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.