Polymorphisms in genes of melatonin biosynthesis and signaling support the light-at-night hypothesis for breast cancer
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Polymorphisms in genes of melatonin biosynthesis and signaling support the light-at-night hypothesis for breast cancer. / Wichert, Katharina; Hoppe, Reiner; Ickstadt, Katja; Behrens, Thomas; Winter, Stefan; Herold, Robert; Terschüren, Claudia; Lo, Wing-Yee; Guénel, Pascal; Truong, Thérèse; Bolla, Manjeet K; Wang, Qin; Dennis, Joe; Michailidou, Kyriaki; Lush, Michael; Andrulis, Irene L; Brenner, Hermann; Chang-Claude, Jenny; Cox, Angela; Cross, Simon S; Czene, Kamila; Eriksson, Mikael; Figueroa, Jonine D; García-Closas, Montserrat; Goldberg, Mark S; Hamann, Ute; He, Wei; Holleczek, Bernd; Hopper, John L; Jakubowska, Anna; Ko, Yon-Dschun; Lubiński, Jan; Mulligan, Anna Marie; Obi, Nadia; Rhenius, Valerie; Shah, Mitul; Shu, Xiao-Ou; Simard, Jacques; Southey, Melissa C; Zheng, Wei; Dunning, Alison M; Pharoah, Paul D P; Hall, Per; Easton, Douglas F; Brüning, Thomas; Brauch, Hiltrud; Harth, Volker; Rabstein, Sylvia.
in: EUR J EPIDEMIOL, Jahrgang 38, Nr. 10, 10.2023, S. 1053-1068.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Polymorphisms in genes of melatonin biosynthesis and signaling support the light-at-night hypothesis for breast cancer
AU - Wichert, Katharina
AU - Hoppe, Reiner
AU - Ickstadt, Katja
AU - Behrens, Thomas
AU - Winter, Stefan
AU - Herold, Robert
AU - Terschüren, Claudia
AU - Lo, Wing-Yee
AU - Guénel, Pascal
AU - Truong, Thérèse
AU - Bolla, Manjeet K
AU - Wang, Qin
AU - Dennis, Joe
AU - Michailidou, Kyriaki
AU - Lush, Michael
AU - Andrulis, Irene L
AU - Brenner, Hermann
AU - Chang-Claude, Jenny
AU - Cox, Angela
AU - Cross, Simon S
AU - Czene, Kamila
AU - Eriksson, Mikael
AU - Figueroa, Jonine D
AU - García-Closas, Montserrat
AU - Goldberg, Mark S
AU - Hamann, Ute
AU - He, Wei
AU - Holleczek, Bernd
AU - Hopper, John L
AU - Jakubowska, Anna
AU - Ko, Yon-Dschun
AU - Lubiński, Jan
AU - Mulligan, Anna Marie
AU - Obi, Nadia
AU - Rhenius, Valerie
AU - Shah, Mitul
AU - Shu, Xiao-Ou
AU - Simard, Jacques
AU - Southey, Melissa C
AU - Zheng, Wei
AU - Dunning, Alison M
AU - Pharoah, Paul D P
AU - Hall, Per
AU - Easton, Douglas F
AU - Brüning, Thomas
AU - Brauch, Hiltrud
AU - Harth, Volker
AU - Rabstein, Sylvia
N1 - © 2023. The Author(s).
PY - 2023/10
Y1 - 2023/10
N2 - Light-at-night triggers the decline of pineal gland melatonin biosynthesis and secretion and is an IARC-classified probable breast-cancer risk factor. We applied a large-scale molecular epidemiology approach to shed light on the putative role of melatonin in breast cancer. We investigated associations between breast-cancer risk and polymorphisms at genes of melatonin biosynthesis/signaling using a study population of 44,405 women from the Breast Cancer Association Consortium (22,992 cases, 21,413 population-based controls). Genotype data of 97 candidate single nucleotide polymorphisms (SNPs) at 18 defined gene regions were investigated for breast-cancer risk effects. We calculated adjusted odds ratios (ORs) and 95% confidence intervals (CI) by logistic regression for the main-effect analysis as well as stratified analyses by estrogen- and progesterone-receptor (ER, PR) status. SNP-SNP interactions were analyzed via a two-step procedure based on logic regression. The Bayesian false-discovery probability (BFDP) was used for all analyses to account for multiple testing. Noteworthy associations (BFDP < 0.8) included 10 linked SNPs in tryptophan hydroxylase 2 (TPH2) (e.g. rs1386492: OR = 1.07, 95% CI 1.02-1.12), and a SNP in the mitogen-activated protein kinase 8 (MAPK8) (rs10857561: OR = 1.11, 95% CI 1.04-1.18). The SNP-SNP interaction analysis revealed noteworthy interaction terms with TPH2- and MAPK-related SNPs (e.g. rs1386483R ∧ rs1473473D ∧ rs3729931D: OR = 1.20, 95% CI 1.09-1.32). In line with the light-at-night hypothesis that links shift work with elevated breast-cancer risks our results point to SNPs in TPH2 and MAPK-genes that may impact the intricate network of circadian regulation.
AB - Light-at-night triggers the decline of pineal gland melatonin biosynthesis and secretion and is an IARC-classified probable breast-cancer risk factor. We applied a large-scale molecular epidemiology approach to shed light on the putative role of melatonin in breast cancer. We investigated associations between breast-cancer risk and polymorphisms at genes of melatonin biosynthesis/signaling using a study population of 44,405 women from the Breast Cancer Association Consortium (22,992 cases, 21,413 population-based controls). Genotype data of 97 candidate single nucleotide polymorphisms (SNPs) at 18 defined gene regions were investigated for breast-cancer risk effects. We calculated adjusted odds ratios (ORs) and 95% confidence intervals (CI) by logistic regression for the main-effect analysis as well as stratified analyses by estrogen- and progesterone-receptor (ER, PR) status. SNP-SNP interactions were analyzed via a two-step procedure based on logic regression. The Bayesian false-discovery probability (BFDP) was used for all analyses to account for multiple testing. Noteworthy associations (BFDP < 0.8) included 10 linked SNPs in tryptophan hydroxylase 2 (TPH2) (e.g. rs1386492: OR = 1.07, 95% CI 1.02-1.12), and a SNP in the mitogen-activated protein kinase 8 (MAPK8) (rs10857561: OR = 1.11, 95% CI 1.04-1.18). The SNP-SNP interaction analysis revealed noteworthy interaction terms with TPH2- and MAPK-related SNPs (e.g. rs1386483R ∧ rs1473473D ∧ rs3729931D: OR = 1.20, 95% CI 1.09-1.32). In line with the light-at-night hypothesis that links shift work with elevated breast-cancer risks our results point to SNPs in TPH2 and MAPK-genes that may impact the intricate network of circadian regulation.
U2 - 10.1007/s10654-023-01048-7
DO - 10.1007/s10654-023-01048-7
M3 - SCORING: Journal article
C2 - 37789226
VL - 38
SP - 1053
EP - 1068
JO - EUR J EPIDEMIOL
JF - EUR J EPIDEMIOL
SN - 0393-2990
IS - 10
ER -
