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Circadian genes polymorphisms, night work and prostate cancer risk: Findings from the EPICAP study
Author(s) -
WendeuFoyet Méyomo G.,
Cénée Sylvie,
Koudou Yves,
Trétarre Brigitte,
Rébillard Xavier,
CancelTassin Géraldine,
Cussenot Olivier,
Boland Anne,
Olaso Robert,
Deleuze JeanFrançois,
Blanché Hélène,
Lamy PierreJean,
Mulot Claire,
LaurentPuig Pierre,
Truong Thérèse,
Menegaux Florence
Publication year - 2020
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.33139
Subject(s) - prostate cancer , circadian rhythm , snp , cancer , odds ratio , oncology , shift work , logistic regression , medicine , single nucleotide polymorphism , biology , population , genetics , genotype , gene , environmental health , neuroscience
Over the past two decades, several studies have attempted to understand the hypothesis that disrupting the circadian rhythm may promote the development of cancer. Some have suggested that night work and some circadian genes polymorphisms are associated with cancer, including prostate cancer. Our study aims to test the hypothesis that prostate cancer risk among night workers may be modulated by genetic polymorphisms in the circadian pathway genes based on data from the EPICAP study, a population‐based case‐control study including 1511 men (732 cases/779 controls) with genotyped data. We estimated odds ratio (ORs) and P values of the association between prostate cancer and circadian gene variants using logistic regression models. We tested the interaction between circadian genes variants and night work indicators that were significantly associated with prostate cancer at pathway, gene and SNP levels. Analyses were also stratified by each of these night work indicators and by cancer aggressiveness. The circadian pathway was significantly associated with aggressive prostate cancer among night workers ( P = .004), particularly for men who worked at night for <20 years ( P = .0002) and those who performed long night shift (>10 hours, P = .001). At the gene level, we observed among night workers significant associations between aggressive prostate cancer and ARNTL , NPAS2 and RORA . At the SNP‐level, no significant association was observed. Our findings provide some clues of a potential modulating effect of circadian genes in the relationship between night work and prostate cancer. Further investigation is warranted to confirm these findings and to better elucidate the biological pathways involved.