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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; Lubinski, 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.
  • Wichert K; Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bürkle-de-la-Camp-Platz 1, 44789, Bochum, Germany. katharina.wichert@dguv.de.
  • Hoppe R; Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, Germany.
  • Ickstadt K; University of Tübingen, Tübingen, Germany.
  • Behrens T; Department of Statistics, TU Dortmund University, Dortmund, Germany.
  • Winter S; Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bürkle-de-la-Camp-Platz 1, 44789, Bochum, Germany.
  • Herold R; Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, Germany.
  • Terschüren C; University of Tübingen, Tübingen, Germany.
  • Lo WY; Institute for Occupational and Maritime Medicine Hamburg (ZfAM), University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
  • Guénel P; Institute for Occupational and Maritime Medicine Hamburg (ZfAM), University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
  • Truong T; Department of Clinical Pathology, University of Melbourne Centre for Cancer Research Victorian Comprehensive Cancer Centre Melbourne, Melbourne, VIC, Australia.
  • Bolla MK; Team "Exposome and Heredity", CESP, Gustave Roussy, INSERM, University Paris-Saclay, UVSQ, Villejuif, France.
  • Wang Q; Team "Exposome and Heredity", CESP, Gustave Roussy, INSERM, University Paris-Saclay, UVSQ, Villejuif, France.
  • Dennis J; Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
  • Michailidou K; Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
  • Lush M; Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
  • Andrulis IL; Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
  • Brenner H; Biostatistics Unit, The Cyprus Institute of Neurology & Genetics, Nicosia, Cyprus.
  • Chang-Claude J; Cyprus School of Molecular Medicine, The Cyprus Institute of Neurology & Genetics, Nicosia, Cyprus.
  • Cox A; Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
  • Cross SS; Fred A. Litwin Center for Cancer Genetics, Lunenfeld-Tanenbaum Research Institute of Mount Sinai Hospital, Toronto, ON, Canada.
  • Czene K; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
  • Eriksson M; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Figueroa JD; Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Heidelberg, Germany.
  • García-Closas M; German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Goldberg MS; Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Hamann U; Cancer Epidemiology Group, University Cancer Center Hamburg (UCCH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
  • He W; Sheffield Institute for Nucleic Acids (SInFoNiA), Department of Oncology and Metabolism, University of Sheffield, Sheffield, UK.
  • Holleczek B; Academic Unit of Pathology, Department of Neuroscience, University of Sheffield, Sheffield, UK.
  • Hopper JL; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
  • Jakubowska A; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
  • Ko YD; Usher Institute of Population Health Sciences and Informatics, The University of Edinburgh, Edinburgh, UK.
  • Lubinski J; Cancer Research UK Edinburgh Centre, The University of Edinburgh, Edinburgh, UK.
  • Mulligan AM; Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
  • Obi N; Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
  • Rhenius V; Department of Medicine, McGill University, Montréal, QC, Canada.
  • Shah M; Division of Clinical Epidemiology, Royal Victoria Hospital, McGill University, Montréal, QC, Canada.
  • Shu XO; Molecular Genetics of Breast Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Simard J; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
  • Southey MC; Saarland Cancer Registry, Saarbrücken, Germany.
  • Zheng W; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia.
  • Dunning AM; Department of Genetics and Pathology, International Hereditary Cancer Center, Pomeranian Medical University, Szczecin, Poland.
  • Pharoah PDP; Independent Laboratory of Molecular Biology and Genetic Diagnostics, Pomeranian Medical University, Szczecin, Poland.
  • Hall P; Department of Internal Medicine, Johanniter GmbH Bonn, Johanniter Krankenhaus, Bonn, Germany.
  • Easton DF; Department of Genetics and Pathology, International Hereditary Cancer Center, Pomeranian Medical University, Szczecin, Poland.
  • Brüning T; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
  • Brauch H; Laboratory Medicine Program, University Health Network, Toronto, ON, Canada.
  • Harth V; Institute for Medical Biometry and Epidemiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
  • Rabstein S; Centre for Cancer Genetic Epidemiology, Department of Oncology, University of Cambridge, Cambridge, UK.
Eur J Epidemiol ; 38(10): 1053-1068, 2023 Oct.
Article en En | MEDLINE | ID: mdl-37789226
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.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Neoplasias de la Mama / Melatonina Tipo de estudio: Risk_factors_studies Límite: Female / Humans Idioma: En Año: 2023 Tipo del documento: Article
Texto completo
Imprimir
XML
PubMed Links
Search on Google

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Neoplasias de la Mama / Melatonina Tipo de estudio: Risk_factors_studies Límite: Female / Humans Idioma: En Año: 2023 Tipo del documento: Article