Evidence map›Paper›PMID 29318656›Full record

Trial reportMolecular carcinogenesis2018

Circadian genes and risk of prostate cancer in the prostate cancer prevention trial.

Lisa W Chu, Cathee Till, Baiyu Yang, Catherine M Tangen, Phyllis J Goodman, Kai Yu, Yong Zhu, Summer Han, Ashraful M Hoque, Christine Ambrosone and 3 more

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Molecular carcinogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-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

13 citing papers in PubMed, 24 citations in OpenAlex.

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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 8 institutions in 1 country.

Lisa W ChuFormerly Cancer Prevention Institute of California, Fremont, California.
Cathee TillSWOG Statistical Center, Seattle, Washington.
Baiyu YangStanford Cancer Institute, Stanford School of Medicine, Stanford, California.ORCID 0000-0002-9326-3736
Catherine M TangenSWOG Statistical Center, Seattle, Washington.
Phyllis J GoodmanSWOG Statistical Center, Seattle, Washington.
Kai YuNational Cancer Institute, Bethesda, MaryLand.
Yong ZhuYale University, New Haven, Connecticut.
Summer HanStanford Cancer Institute, Stanford School of Medicine, Stanford, California.
Ashraful M HoqueMD Anderson Cancer Center, Houston, Texas.
Christine AmbrosoneRoswell Park Cancer Institute, Buffalo, New York.
Ian ThompsonFormerly University of Texas Health Science Center, San Antonio, Texas.
Robin LeachFormerly University of Texas Health Science Center, San Antonio, Texas.
Ann W HsingFormerly Cancer Prevention Institute of California, Fremont, California.
Cancer Research And Biostatistics · USCancer Prevention Institute of California · USStanford Medicine · USThe University of Texas Health Science Center at San Antonio · USNational Cancer Institute · USRoswell Park Comprehensive Cancer Center · USThe University of Texas MD Anderson Cancer Center · USYale University · US

Funding

SWOG Foreign AccrualsU10CA037429 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BLANKE, CHARLES D., MEYSKENS, FRANK L. · 1985 to 2014
$205.2M
SWOG NCORP Research BaseUG1CA189974 · NCI · THE HOPE FOUNDATION · PI CHARLES D. BLANKE, DAWN HERSHMAN · 2014 to 2026
$80.6M
PCPT and SELECT cohorts: Core Infrastructure Support for Cancer Research UM1CA182883 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TANGEN, CATHERINE M., THOMPSON, IAN M. · 2013 to 2017
$5.2M
NCI NIH HHS U10 CA037429NCI NIH HHS UG1 CA189974NCI NIH HHS UM1 CA182883
6 · The paper itself

Abstract

Circadian genes have been considered as a possible biological mechanism for the observed relationship between circadian rhythm disruptions and increased risk of hormone-related cancers. In the current study, we investigated the relationship between circadian gene variants and prostate cancer risk and whether reducing bioavailable testosterone modifies the circadian genes-prostate cancer relationship. We conducted a nested case-control study among Caucasian men in the Prostate Cancer Prevention Trial (PCPT), a randomized placebo-controlled clinical trial to assess if finasteride (an androgen bioactivation inhibitor) could prevent prostate cancer. We evaluated the associations between 240 circadian gene variations and prostate cancer risk among 1092 biopsy-confirmed prostate cancer cases and 1089 biopsy-negative controls in the study (642 cases and 667 controls from the placebo group; 450 cases and 422 controls from the finasteride group), stratified by treatment group. Among men in the finasteride group, there were suggestive associations between NPAS2 variants and total prostate cancer risk, with one SNP remaining statistically significant after Bonferroni correction (rs746924, odds ratio [OR] = 1.5, P = 9.6 × 10

Indexed as

Polymorphism, Single Nucleotide5-alpha Reductase InhibitorsAgedBasic Helix-Loop-Helix ProteinsCase-Control StudiesCircadian ClocksFinasterideHumansMaleMiddle AgedNerve Tissue ProteinsProstateProstatic NeoplasmsRisk Factors5-alpha Reductase InhibitorsBasic Helix-Loop-Helix ProteinsFinasterideNerve Tissue ProteinsNPAS2 protein, humancircadian genesfinasteridegenetic polymorphismsprostate cancerprostate cancer prevention trial

Identifiers

PMID29318656
PMCPMC5940353
OpenAlexW2782765576

What OpenQuestion holds

Textmetadata
LicenceTDM
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.