Circadian gene variants and breast cancer

被引:45
作者
Reszka, Edyta [1 ]
Przybek, Monika [1 ]
Muurlink, Olav [2 ,3 ]
Peplonska, Beata [4 ]
机构
[1] Nofer Inst Occupat Med, Dept Mol Genet & Epigenet, Teresy St 8, PL-91348 Lodz, Poland
[2] Cent Queensland Univ, 160 Ann St, Brisbane, Qld, Australia
[3] Griffith Inst Educ Res, 76 Messines Ridge Rd, Mt Gravatt, Qld, Australia
[4] Nofer Inst Occupat Med, Dept Environm Epidemiol, Teresy St 8, PL-91348 Lodz, Poland
关键词
Circadian genes; Clock genes; Genetic polymorphism; Breast cancer; Shift work; CLOCK-3111 T/C SNP; NIGHT-SHIFT WORK; 3'-UNTRANSLATED REGION; LENGTH POLYMORPHISM; FEEDBACK-REGULATION; EVENING PREFERENCE; RISK; ASSOCIATION; DISRUPTION; NPAS2;
D O I
10.1016/j.canlet.2017.01.012
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The endogenous and self-sustained circadian rhythm generated and maintained in suprachiasmatic nucleus and peripheral tissues can coordinate various molecular, biochemical and physiological processes in living organisms resulting in the adaptation to environmental cues, e.g. light. Multifactorial breast cancer etiology also involves circadian gene alterations, especially among individuals exposed to light at night. Indeed, shift work that causes circadian disruption has been classified by the International Agency for Research on Cancer as a probable human carcinogen, group 2A. Thus it seems extremely important to recognize specific susceptible gene variants among around 20 candidate circadian genes that may be linked with breast cancer etiology. The aim of this review was to evaluate recent data investigating a putative link between circadian gene polymorphisms and breast cancer risk. We summarize fifteen epidemiological studies, including five studies on shift work that have indicated BMAL1, BMAL2, CLOCK, NPAS2, CRY1, CRY2, PERI, PER3 and TIMELESS as a candidate breast cancer risk variants. (C) 2017 Elsevier B.V. All rights reserved.
引用
收藏
页码:137 / 145
页数:9
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