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1. Alcohol consumption, cigarette smoking, and risk of breast cancer for BRCA1 and BRCA2 mutation carriers: results from The BRCA1 and BRCA2 Cohort Consortium

Author

Terry, Mary Beth, Noguès, Catherine, Barrowdale, Daniel, Frost, Debra, Brewer, Carole, Evans, D. Gareth, Izatt, Louise, Side, Lucy, Walker, Lisa, Tischkowitz, Marc, Rogers, Mark, Porteous, Mary, Meijers-Heijboer, Hanne E.J., Gille, Johan JP, Blok, Marinus, Hoogerbrugge, Nicoline, Daly, Mary, Andrulis, Irene, Buys, Saundra, John, Esther, McLachlan, Sue-Anne, Friedlander, Michael, Tan, Yen, Osorio, Ana, Caldés, Trinidad, Jakubowska, Anna, Simard, Jacques, Singer, Christian, Olah, Edith, Navratilova, Marie, Foretova, Lenka, Gerdes, Anne-Marie, Roos-Blom, Marie-José, Arver, Brita, Olsson, Håkan, Schmutzler, Rita, Hopper, John, Milne, Roger, Easton, Douglas, Van Leeuwen, Flora, Rookus, Matti, Andrieu, Nadine, Goldgar, David, Huntsman Cancer Institute [Salt Lake City], University of Utah, Laboratoire d'Oncogénétique, CRLCC René Huguenin, Centre for Cancer Genetic Epidemiology, University of Cambridge [UK] (CAM), Department of Clinical Genetics, Royal Devon & Exeter Hospital, Genetic Medicine, St Mary's Hospital, Manchester Academic Health Sciences Centre, University of Manchester, Clinical Genetics, Guy's and St. Thomas' NHS Foundation Trust, Department of Clinical Genetics, The Churchill, Oxford, Oxford Regional Genetics Service [Oxford, UK], Churchill Hospital Oxford Centre for Haematology, Department of Genetics, Portuguese Oncology Institute, Department of Computer Science [Colorado State University], Colorado State University [Fort Collins] (CSU), West General Hospital, VU University Medical Center [Amsterdam], University Hospital Maastricht, Department of Human Genetics, Radboud University Medical Center [Nijmegen], Division of Population Science, Fox Chase Cancer Center, Department of Laboratory Medicine and Pathobiology, University of Toronto, Department of Internal Medicine, Huntsman Cancer Institute, Department of Epidemiology, Cancer Prevention Institute of California, St. Vincent's Hospital, Sydney, Dept of Medical Oncology, Division of Medicine, University of New South Wales [Sydney] (UNSW)-Prince of Wales Hospital Randwick, Medical University of Vienna, Human Genetics Group, Spanish National Cancer Research Centre, Molecular Oncology Laboratory, Hospital Clínico San Carlos, Department of Genetics and Pathology, Pomeranian Medical University-International Hereditary Cancer Centre, Laboratoire de Génomique des Cancers, Laval University [Québec], Division of Special Gynecology, Medizinische Universität Wien = Medical University of Vienna-Department of OB/GYN, National Institute of Oncology, Masaryk Memorial Cancer Institute (RECAMO), Odense University Hospital, Netherlands Cancer Institute (NKI), Antoni van Leeuwenhoek Hospital, Radiumhemmet, Karolinska University Hospital [Stockholm], Department of Oncology, Lund University Hospital, Division of Molecular Gyneco-Oncology, Department of Gynaecology and Obstetrics, Clinical Center Un, Centre for MEGA Epidemiology, The University of Melbourne, Victoria, Australia, Cancer Epidemiology Centre, Cancer Council Victoria, Centre for Cancer Genetic Epidemiology [Cambridge], Department of Oncology-University of Cambridge [UK] (CAM), Departments of Epidemiology and Molecular Pathology, The Netherlands Cancer Institute, Netherlands Cancer Institute, Innovation et Développement dans l'Agriculture et l'Agro-alimentaire (Innovation), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Centre national d'études agronomiques des régions chaudes (CNEARC)-Institut National de la Recherche Agronomique (INRA)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Centre International de Hautes Etudes Agronomiques Méditerranéennes - Institut Agronomique Méditerranéen de Montpellier (CIHEAM-IAMM), Centre International de Hautes Études Agronomiques Méditerranéennes (CIHEAM)-Centre International de Hautes Études Agronomiques Méditerranéennes (CIHEAM)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), Department of Dermatology [Salt Lake City, UT, USA], University of Utah School of Medicine [Salt Lake City], This work was supported by grants to kConFab and the kConFab Follow-Up Study from Cancer Australia (809195, 1100868), the Australian National Breast Cancer Foundation (IF 17), the National Health and Medical Research Council (454508, 288704, 145684), the National Institute of Health U.S.A. (1RO1CA159868), the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania and South Australia, and the Cancer Foundation of Western Australia. Kelly Phillips is an Australian National Breast Cancer Foundation fellow.Lenka Foretova was supported by MH CZ - DRO (MMCI, 00209805) and by MEYS - NPS I- LO1413 to LF, MN. Edith Olah and The Hungarian Breast and Ovarian Cancer Study was supported by Hungarian Research Grants KTIA-OTKA CK-80745, NKFI OTKA K-112228 and the Norwegian EEA Financial Mechanism HU0115/NA/2008-3/ÖP-9. Hakan Olsson and Lund-BRCA collaborators are supported by the Swedish Cancer Society, Lund Hospital Funds, and European Research Council Advanced Grant ERC-2011-294576. Stockholm-BRCA collaborators are supported by the Swedish Cancer Society., Medizinische Universität Wien = Medical University of Vienna, Université Laval [Québec] (ULaval), Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie [Paris], MINES ParisTech - École nationale supérieure des mines de Paris, and Université Paris sciences et lettres (PSL)

Subjects
breast cancer, endocrine system diseases, alcohol, cigarette smoking, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, skin and connective tissue diseases, BRCA1, BRCA2
Abstract

International audience; BACKGROUND:Tobacco smoking and alcohol consumption have been intensively studied in the general population to assess their effects on the risk of breast cancer (BC), but very few studies have examined these effects in BRCA1 and BRCA2 mutation carriers. Given the high BC risk for mutation carriers and the importance of BRCA1 and BRCA2 in DNA repair, better evidence on the associations of these lifestyle factors with BC risk is essential.METHODS:Using a large international pooled cohort of BRCA1 and BRCA2 mutation carriers, we conducted retrospective (5,707 BRCA1 mutation carriers; 3,525 BRCA2 mutation carriers) and prospective (2,276 BRCA1 mutation carriers; 1,610 BRCA2 mutation carriers) analyses of alcohol and tobacco consumption using Cox proportional hazards models.RESULTS:For both BRCA1 and BRCA2 mutation carriers, none of the smoking-related variables was associated with BC risk, except smoking for more than five years before a first full-term pregnancy (FFTP) when compared to parous women who never smoked. For BRCA1 mutation carriers, the HR from retrospective analysis (HRR) was 1.19 (95%CI:1.02,1.39) and the HR from prospective analysis (HRP) was 1.36 (95%CI:0.99,1.87). For BRCA2 mutation carriers, smoking for more than five years before a FFTP showed an association of a similar magnitude, but the confidence limits were wider (HRR=1.25,95%CI:1.01,1.55 and HRP=1.30,95%CI:0.83,2.01). For both carrier groups, alcohol consumption was not associated with BC risk.CONCLUSIONS:The finding that smoking during the pre-reproductive years increases BC risk for mutation carriers warrants further investigation.IMPACT:This is the largest prospective study of BRCA mutation carriers to assess these important risk factors.

Published
2019
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2. Alcohol consumption, cigarette smoking, and risk of breast cancer for BRCA1 and BRCA2 mutation carriers: results from The BRCA1 and BRCA2 Cohort Consortium: Alcohol and smoking and breast cancer risk for BRCA carriers

Author

Terry, Mary Beth, Noguès, Catherine, Barrowdale, Daniel, Frost, Debra, Brewer, Carole, Evans, D. Gareth, Izatt, Louise, Side, Lucy, Walker, Lisa, Tischkowitz, Marc, Rogers, Mark, Porteous, Mary, Meijers-Heijboer, Hanne E.J., Gille, Johan Jp, Blok, Marinus, Hoogerbrugge, Nicoline, Daly, Mary, Andrulis, Irene, Buys, Saundra, John, Esther, Mclachlan, Sue-Anne, Friedlander, Michael, Tan, Yen, Osorio, Ana, Caldés, Trinidad, Jakubowska, Anna, Simard, Jacques, Singer, Christian, Olah, Edith, Navratilova, Marie, Foretova, Lenka, Gerdes, Anne-Marie, Roos-Blom, Marie-José, Arver, Brita, Olsson, Håkan, Schmutzler, Rita, Hopper, John, Milne, Roger, Easton, Douglas, van Leeuwen, Flora, Rookus, Matti, Andrieu, Nadine, Goldgar, David, Andrieu, Nadine, Huntsman Cancer Institute [Salt Lake City], University of Utah, Laboratoire d'Oncogénétique, CRLCC René Huguenin, Centre for Cancer Genetic Epidemiology, University of Cambridge [UK] (CAM), Department of Clinical Genetics, Royal Devon & Exeter Hospital, Genetic Medicine, St Mary's Hospital, Manchester Academic Health Sciences Centre, University of Manchester, Clinical Genetics, Guy's and St. Thomas' NHS Foundation Trust, Department of Clinical Genetics, The Churchill, Oxford, Oxford Regional Genetics Service [Oxford, UK], Churchill Hospital Oxford Centre for Haematology, Department of Genetics, Portuguese Oncology Institute, Department of Computer Science [Colorado State University], Colorado State University [Fort Collins] (CSU), West General Hospital, VU University Medical Center [Amsterdam], University Hospital Maastricht, Department of Human Genetics, Radboud University Medical Center [Nijmegen], Division of Population Science, Fox Chase Cancer Center, Department of Laboratory Medicine and Pathobiology, University of Toronto, Department of Internal Medicine, Huntsman Cancer Institute, Department of Epidemiology, Cancer Prevention Institute of California, St. Vincent's Hospital, Sydney, Dept of Medical Oncology, Division of Medicine, University of New South Wales [Sydney] (UNSW)-Prince of Wales Hospital Randwick, Medizinische Universität Wien = Medical University of Vienna, Human Genetics Group, Spanish National Cancer Research Centre, Molecular Oncology Laboratory, Hospital Clínico San Carlos, Department of Genetics and Pathology, International Hereditary Cancer Centre-Pomeranian Medical University [Szczecin] (PUM), Laboratoire de Génomique des Cancers, Université Laval [Québec] (ULaval), Division of Special Gynecology, Medizinische Universität Wien = Medical University of Vienna-Department of OB/GYN, National Institute of Oncology, Masaryk Memorial Cancer Institute (MMCI), Odense University Hospital, Netherlands Cancer Institute (NKI), Antoni van Leeuwenhoek Hospital, Radiumhemmet, Karolinska University Hospital [Stockholm], Department of Oncology, Lund University Hospital, Division of Molecular Gyneco-Oncology, Department of Gynaecology and Obstetrics, Clinical Center Un, Centre for MEGA Epidemiology, The University of Melbourne, Victoria, Australia, Cancer Epidemiology Centre, Cancer Council Victoria, Centre for Cancer Genetic Epidemiology [Cambridge], University of Cambridge [UK] (CAM)-Department of Oncology, Departments of Epidemiology and Molecular Pathology, The Netherlands Cancer Institute, Netherlands Cancer Institute, Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie [Paris], Mines Paris - PSL (École nationale supérieure des mines de Paris), Université Paris sciences et lettres (PSL), Department of Dermatology [Salt Lake City, UT, USA], University of Utah School of Medicine [Salt Lake City], and This work was supported by grants to kConFab and the kConFab Follow-Up Study from Cancer Australia (809195, 1100868), the Australian National Breast Cancer Foundation (IF 17), the National Health and Medical Research Council (454508, 288704, 145684), the National Institute of Health U.S.A. (1RO1CA159868), the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania and South Australia, and the Cancer Foundation of Western Australia. Kelly Phillips is an Australian National Breast Cancer Foundation fellow.Lenka Foretova was supported by MH CZ - DRO (MMCI, 00209805) and by MEYS - NPS I- LO1413 to LF, MN. Edith Olah and The Hungarian Breast and Ovarian Cancer Study was supported by Hungarian Research Grants KTIA-OTKA CK-80745, NKFI OTKA K-112228 and the Norwegian EEA Financial Mechanism HU0115/NA/2008-3/ÖP-9. Hakan Olsson and Lund-BRCA collaborators are supported by the Swedish Cancer Society, Lund Hospital Funds, and European Research Council Advanced Grant ERC-2011-294576. Stockholm-BRCA collaborators are supported by the Swedish Cancer Society.

Subjects
breast cancer, endocrine system diseases, alcohol, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, cigarette smoking, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, skin and connective tissue diseases, BRCA1, BRCA2
Abstract

International audience; BACKGROUND:Tobacco smoking and alcohol consumption have been intensively studied in the general population to assess their effects on the risk of breast cancer (BC), but very few studies have examined these effects in BRCA1 and BRCA2 mutation carriers. Given the high BC risk for mutation carriers and the importance of BRCA1 and BRCA2 in DNA repair, better evidence on the associations of these lifestyle factors with BC risk is essential.METHODS:Using a large international pooled cohort of BRCA1 and BRCA2 mutation carriers, we conducted retrospective (5,707 BRCA1 mutation carriers; 3,525 BRCA2 mutation carriers) and prospective (2,276 BRCA1 mutation carriers; 1,610 BRCA2 mutation carriers) analyses of alcohol and tobacco consumption using Cox proportional hazards models.RESULTS:For both BRCA1 and BRCA2 mutation carriers, none of the smoking-related variables was associated with BC risk, except smoking for more than five years before a first full-term pregnancy (FFTP) when compared to parous women who never smoked. For BRCA1 mutation carriers, the HR from retrospective analysis (HRR) was 1.19 (95%CI:1.02,1.39) and the HR from prospective analysis (HRP) was 1.36 (95%CI:0.99,1.87). For BRCA2 mutation carriers, smoking for more than five years before a FFTP showed an association of a similar magnitude, but the confidence limits were wider (HRR=1.25,95%CI:1.01,1.55 and HRP=1.30,95%CI:0.83,2.01). For both carrier groups, alcohol consumption was not associated with BC risk.CONCLUSIONS:The finding that smoking during the pre-reproductive years increases BC risk for mutation carriers warrants further investigation.IMPACT:This is the largest prospective study of BRCA mutation carriers to assess these important risk factors.

Published
2019
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3. The Influence of Number and Timing of Pregnancies on Breast Cancer Risk for Women With BRCA1 or BRCA2 Mutations

Author

Douglas F. Easton, T.M. Mooij, Christian F. Singer, Lenka Foretova, Matti A. Rookus, Karin Kast, Kai-ren Ong, Louise Izatt, Jessica Moretta-Serra, Margreet G. E. M. Ausems, Diana Eccles, Patrick J. Morrison, Jan C. Oosterwijk, Mary B. Daly, Alex Henderson, Rita K. Schmutzler, Ana Osorio, Charlotte J. Dommering, Anne-Marie Gerdes, Marie Navratilova, Ibccs, Carole Brewer, Mieke Kriege, Mary Beth Terry, Christoph Engel, D. Gareth Evans, Edith Olah, Jackie Cook, David E. Goldgar, Anna Jakubowska, Antonis C. Antoniou, Jacques Simard, Laurence Gladieff, Catherine Noguès, Esther M. John, Brita Arver, Håkan Olsson, Jasmine A. McDonald, Irene L. Andrulis, Nadine Andrieu, Munaza Ahmed, Yen Y. Tan, Yuyan Liao, Embrace, Genepso, Bcfr, Hebon, kConFab, Trinidad Caldés, Véronique Mari, Roger L. Milne, Michael Friedlander, Elisabeth Luporsi, John L. Hopper, Marie-José Roos-Blom, Flora E. van Leeuwen, Sue-Anne McLachlan, Saundra S. Buys, Debra Frost, Daniel Barrowdale, Bruno Buecher, Department of Epidemiology [Columbia University], Columbia University [New York]-Columbia Mailman School of Public Health, Columbia University [New York], Department of Gynaecology and Obstetrics, University Hospital Carl Gustav Carus, Centre for Cancer Genetic Epidemiology, University of Cambridge [UK] (CAM), Institute for Medical Informatics, Statistics and Epidemiology [Leipzig] (IMISE), Universität Leipzig, Laboratoire d'Oncogénétique, CRLCC René Huguenin, Service de Génétique Oncologique, Institut Curie [Paris], Centre de Lutte contre le Cancer Antoine Lacassagne [Nice] (UNICANCER/CAL), UNICANCER-Université Côte d'Azur (UCA), Institut Claudius Regaud, Centre Alexis Vautrin (CAV), Newcastle Upon Tyne Hospitals NHS Trust, Department of Clinical Genetics, Royal Devon & Exeter Hospital, St Mary's Hospital, Wessex Clinical Genetics Service, Princess Anne Hospital, Sheffield Clinical Genetics Service, Sheffield Children's NHS Foundation Trust, West Midlands Regional Genetics Service, Birmingham Women's and Children's NHS Foundation Trust, Clinical Genetics, Guy's and St. Thomas' NHS Foundation Trust, Northern Ireland Regional Genetics Centre, Belfast City Hospital, Department of Clinical Genetics and Human Genetics, VU University Medical Center [Amsterdam], Department of Genetics, Department of Medical Genetics, University Medical Center [Utrecht], Erasmus University Medical Center [Rotterdam] (Erasmus MC)-Family Cancer Clinic, Department of Internal Medicine, Huntsman Cancer Institute, Department of Laboratory Medicine and Pathobiology, University of Toronto, Department of Epidemiology, Cancer Prevention Institute of California, Division of Population Science, Fox Chase Cancer Center, Dept of Medical Oncology, Division of Medicine, University of New South Wales [Sydney] (UNSW)-Prince of Wales Hospital Randwick, Human Genetics Group, Spanish National Cancer Research Centre, Molecular Oncology Laboratory, Hospital Clínico San Carlos, Department of Genetics and Pathology, International Hereditary Cancer Centre-Pomeranian Medical University [Szczecin] (PUM), Laboratoire de Génomique des Cancers, Université Laval [Québec] (ULaval), Division of Special Gynecology, Medizinische Universität Wien = Medical University of Vienna-Department of OB/GYN, National Institute of Oncology, Masaryk University [Brno] (MUNI), Odense University Hospital, Radiumhemmet, Karolinska University Hospital [Stockholm], Department of Oncology, Lund University Hospital, Division of Molecular Gyneco-Oncology, Department of Gynaecology and Obstetrics, Clinical Center Un, Centre for MEGA Epidemiology, The University of Melbourne, Victoria, Australia, Departments of Epidemiology and Molecular Pathology, The Netherlands Cancer Institute, Department of Dermatology, University of Utah School of Medicine [Salt Lake City], Cancer Epidemiology Centre, Cancer Council Victoria, Centre for Cancer Genetic Epidemiology [Cambridge], University of Cambridge [UK] (CAM)-Department of Oncology, Netherlands Cancer Institute, Innovation et Développement dans l'Agriculture et l'Alimentation (UMR Innovation), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Institut National de la Recherche Agronomique (INRA)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), This work was supported by grants to kConFab and the kConFab Follow-Up Study from Cancer Australia (809195), the Australian National Breast Cancer Foundation (IF 17), the National Health and Medical Research Council (454508, 288704, 145684), the US National Institute of Health (1RO1CA159868), the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania, and South Australia, and the Cancer Foundation of Western Australia. MODSQUAD Czech Republic, Brno was supported by MH CZ—DRO (MMCI, 00209805) and by MEYS—NPS I - LO1413 to LF, MN. The Hungarian Breast and Ovarian Cancer Study was supported by Hungarian Research grants KTIA-OTKA CK80745 and NKFI OTKA K-112228 and the Norwegian EEA Financial Mechanism HU0115/NA/2008-3/OP-9. € Lund-BRCA collaborators are supported by the Swedish Cancer Society, Lund Hospital Funds, and European Research Council Advanced grant ERC-2011-294576. Stockholm-BRCA collaborators are supported by the Swedish Cancer Society., European Project: 294576,EC:FP7:ERC,ERC-2011-ADG_20110310,RISK FACTORS CANCER(2012), Klinische Genetica, RS: GROW - R4 - Reproductive and Perinatal Medicine, MUMC+: DA KG Polikliniek (9), MUMC+: DA KG Lab Centraal Lab (9), Universität Leipzig [Leipzig], Institut Curie, Centre Antoine Lacassagne, CRLCC Antoine Lacassagne, CRLCC Institut Claudius Regaud, Sheffield Children's Hospital, Birmingham Women's Hospital Healthcare NHS Trust, Pomeranian Medical University-International Hereditary Cancer Centre, Laval University [Québec], Masaryk Memorial Cancer Institute and Medical Faculty of Masaryk University, Innovation et Développement dans l'Agriculture et l'Agro-alimentaire (Innovation), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Centre national d'études agronomiques des régions chaudes (CNEARC)-Institut National de la Recherche Agronomique (INRA)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Centre International de Hautes Etudes Agronomiques Méditerranéennes - Institut Agronomique Méditerranéen de Montpellier (CIHEAM-IAMM), Centre International de Hautes Études Agronomiques Méditerranéennes (CIHEAM)-Centre International de Hautes Études Agronomiques Méditerranéennes (CIHEAM)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), Andrieu, Nadine, Genetic and environmental risk factors for common malignant tumours especially breast cancer and melanoma. - RISK FACTORS CANCER - - EC:FP7:ERC2012-04-01 - 2017-03-31 - 294576 - VALID, Medical Oncology, Pathology, Radiology & Nuclear Medicine, Columbia Mailman School of Public Health-Columbia University [New York], Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro)-Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro), Targeted Gynaecologic Oncology (TARGON), and Damage and Repair in Cancer Development and Cancer Treatment (DARE)

Subjects
0301 basic medicine, Cancer Research, medicine.medical_specialty, INDUCED-ABORTION, endocrine system diseases, BIRTH, [SDV]Life Sciences [q-bio], [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.GEN] Life Sciences [q-bio]/Genetics, SUSCEPTIBILITY, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, SDG 3 - Good Health and Well-being, [SDV.CAN] Life Sciences [q-bio]/Cancer, Medicine, COHORT, Prospective cohort study, skin and connective tissue diseases, REPRODUCTIVE FACTORS, [SDV.GEN]Life Sciences [q-bio]/Genetics, PARITY, business.industry, Proportional hazards model, Obstetrics, Hazard ratio, Retrospective cohort study, medicine.disease, CARRIERS, OVARIAN, Confidence interval, [SDV] Life Sciences [q-bio], KCONFAB, 030104 developmental biology, Oncology, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, 030220 oncology & carcinogenesis, Cohort, COLLABORATIVE REANALYSIS, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, business, Breast feeding
Abstract

Background Full-term pregnancy (FTP) is associated with a reduced breast cancer (BC) risk over time, but women are at increased BC risk in the immediate years following an FTP. No large prospective studies, however, have examined whether the number and timing of pregnancies are associated with BC risk for BRCA1 and BRCA2 mutation carriers. Methods Using weighted and time-varying Cox proportional hazards models, we investigated whether reproductive events are associated with BC risk for mutation carriers using a retrospective cohort (5707 BRCA1 and 3525 BRCA2 mutation carriers) and a prospective cohort (2276 BRCA1 and 1610 BRCA2 mutation carriers), separately for each cohort and the combined prospective and retrospective cohort. Results For BRCA1 mutation carriers, there was no overall association with parity compared with nulliparity (combined hazard ratio [HRc] = 0.99, 95% confidence interval [CI] = 0.83 to 1.18). Relative to being uniparous, an increased number of FTPs was associated with decreased BC risk (HRc = 0.79, 95% CI = 0.69 to 0.91; HRc = 0.70, 95% CI = 0.59 to 0.82; HRc = 0.50, 95% CI = 0.40 to 0.63, for 2, 3, and ≥4 FTPs, respectively, Ptrend < .0001) and increasing duration of breastfeeding was associated with decreased BC risk (combined cohort Ptrend = .0003). Relative to being nulliparous, uniparous BRCA1 mutation carriers were at increased BC risk in the prospective analysis (prospective hazard ration [HRp] = 1.69, 95% CI = 1.09 to 2.62). For BRCA2 mutation carriers, being parous was associated with a 30% increase in BC risk (HRc = 1.33, 95% CI = 1.05 to 1.69), and there was no apparent decrease in risk associated with multiparity except for having at least 4 FTPs vs. 1 FTP (HRc = 0.72, 95% CI = 0.54 to 0.98). Conclusions These findings suggest differential associations with parity between BRCA1 and BRCA2 mutation carriers with higher risk for uniparous BRCA1 carriers and parous BRCA2 carriers.

Published
2018
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4. An Information-Theoretic Analysis of Genetics, Gender and Age in Cancer Patients

Author

Louise C. Strong, Arnold J. Levine, Mariëlle W. G. Ruijs, Laura J. van't Veer, Thierry Frebourg, Heli Nevanlinna, Gareth L. Bond, Raul Rabadan, Gaëlle Bougeard, Johanna Tommiska, Guillermina Lozano, Marjanka K. Schmidt, Gurinder S. Atwal, Kristiina Aittomäki, Human genetics, CCA - Quality of life, Women's Health Research Program, Department of Obstetrics and Gynecology, School of Biomedical Sciences and Department of Molecular Genetics, Section of Cancer Genetics, The University of Texas M.D. Anderson Cancer Center [Houston], Netherlands Cancer Institute (NKI), Antoni van Leeuwenhoek Hospital, Departments of Epidemiology and Molecular Pathology, The Netherlands Cancer Institute, Department of Obstetrics and Gynaecology, Helsinki University Central Hospital, University of Helsinki, Department of Clinical Genetics, Génomique et Médecine Personnalisée du Cancer et des Maladies Neuropsychiatriques (GPMCND), Université de Rouen Normandie (UNIROUEN), and Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
MESH: Signal Transduction, Male, MESH: Genes, p53, lcsh:Medicine, 312 Clinical medicine, medicine.disease_cause, Bioinformatics, Germline, Prostate cancer, 0302 clinical medicine, Neoplasms, MESH: Germ-Line Mutation, MESH: Neoplasms, MESH: Genetic Variation, lcsh:Science, MESH: Models, Theoretical, Genetics, Sex Characteristics, 0303 health sciences, Multidisciplinary, MESH: Genetic Predisposition to Disease, Age Factors, 3. Good health, Phenotype, 030220 oncology & carcinogenesis, Obstetrics and gynecology, Female, MESH: Sex Characteristics, Research Article, Signal Transduction, MESH: Mutation, education, Biology, MESH: Phenotype, 03 medical and health sciences, Sex Factors, Breast cancer, Germline mutation, MESH: Sex Factors, Heredity, medicine, Humans, Genetic Predisposition to Disease, Genetics and Genomics/Cancer Genetics, Germ-Line Mutation, 030304 developmental biology, MESH: Age Factors, MESH: Humans, Cancer prevention, lcsh:R, Genetic Variation, Models, Theoretical, Genes, p53, medicine.disease, MESH: Male, MESH: Medical Informatics, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, Mutation, lcsh:Q, Mathematics/Statistics, Age of onset, Carcinogenesis, MESH: Female, Medical Informatics
Abstract

International audience; Germline genetics, gender and hormonal-signaling pathways are all well described modifiers of cancer risk and progression. Although an improved understanding of how germline genetic variants interact with other cancer risk factors may allow better prevention and treatment of human cancer, measuring and quantifying these interactions is challenging. In other areas of research, Information Theory has been used to quantitatively describe similar multivariate interactions. We implemented a novel information-theoretic analysis to measure the joint effect of a high frequency germline genetic variant of the p53 tumor suppressor pathway (MDM2 SNP309 T/G) and gender on clinical cancer phenotypes. This analysis quantitatively describes synergistic interactions among gender, the MDM2 SNP309 locus, and the age of onset of tumorigenesis in p53 mutation carriers. These results offer a molecular and genetic basis for the observed sexual dimorphism of cancer risk in p53 mutation carriers and a model is proposed that suggests a novel cancer prevention strategy for p53 mutation carriers.

Published
2008
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5. Effect of chest X-rays on the risk of breast cancer among BRCA1/2 mutation carriers in the international BRCA1/2 carrier cohort study: a report from the EMBRACE, GENEPSO, GEO-HEBON, and IBCCS Collaborators' Group

Author

Douglas F. Easton, Teresa Wagner, Matti A. Rookus, Jenny Chang-Claude, Jean Pierre Fricker, Antonis C. Antoniou, Jacques Simard, Laura J. van't Veer, Elisabeth Cardis, Nadine Andrieu, Susan Peock, David E. Goldgar, Catherine Noguès, Gareth Evans, Flora E. van Leeuwen, Richard M. Brohet, Méthodologie statistique et épidémiologie génétique des maladies multifactorielles, Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Biostatistique, Institut Curie [Paris], Genetic Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge [UK] (CAM), Division of Clinical Epidemiology, German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ), Departments of Epidemiology and Molecular Pathology, The Netherlands Cancer Institute, International Agency for Cancer Research (IACR), Department of Obstetrics and Gynecology, University of Frauenheilkunde, Laboratoire de Génomique des Cancers, Université Laval [Québec] (ULaval), Department of Genetics, St Mary's Hospital, Centre Paul Strauss, CRLCC Paul Strauss, Laboratoire d'Oncogénétique, CRLCC René Huguenin, Department of Medical Informatics, University of Utah, Supported by Grants No. SI2.328176 and SPC.2002482 from the European Commission (International BRCA1/2 Carrier Cohort Study), Cancer Research UK and The British Council (Epidemiological Study of BRCA1 and BRCA2 Mutation Carriers [EMBRACE]), Fondation de France and Ligue Nationale Contre le Cancer (GENEPSO), Dutch Cancer Society Grant No. NKI98-1854 (GEO-HEBON), and the Interdisciplinary Health Research International Team on Breast Cancer Susceptibility (INHERIT) project of the Canadian Institutes of Health Research., EMBRACE, GENEPSO, GEO-HEBON, IBCCS Collaborators' Group, and Andrieu, Nadine

Subjects
Oncology, Cancer Research, medicine.medical_specialty, Population, MESH: Mammography, 030218 nuclear medicine & medical imaging, MESH: Proportional Hazards Models, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, Internal medicine, MESH: Germ-Line Mutation, medicine, MESH: Mass Screening, Risk factor, education, MESH: Cohort Studies, MESH: Heterozygote, Gynecology, education.field_of_study, MESH: Humans, MESH: Middle Aged, MESH: Retros, business.industry, Proportional hazards model, MESH: Questionnaires, Hazard ratio, MESH: Genetic Predisposition to Disease, Retrospective cohort study, MESH: Adult, medicine.disease, 3. Good health, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, 030220 oncology & carcinogenesis, Cohort, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Europe, business, MESH: Female, MESH: Genes, BRCA1, MESH: Breast Neoplasms, MESH: Genes, BRCA2, Cohort study
Abstract

Purpose Women who carry germline mutations in the BRCA1 and BRCA2 genes are at greatly increased risk of breast cancer (BC). Numerous studies have shown that moderate to high doses of ionizing radiation are a risk factor for BC. Because of the role of the BRCA proteins in DNA repair, we hypothesized that BRCA carriers might be more sensitive to ionizing radiation than women in the general population. Patients and Methods A retrospective cohort study of 1,601 female BRCA1/2 carriers was performed. Risk of breast cancer from exposure to chest x-rays, as assessed by questionnaire data, was analyzed using a weighted Cox proportional hazards model. Results In this cohort, any reported exposure to chest x-rays was associated with an increased risk of BC (hazard ratio [HR] = 1.54; P = .007). This risk was increased in carrier women aged 40 years and younger (HR = 1.97; P < .001) and in women born after 1949 (HR = 2.56; P < .001), particularly those exposed only before the age of 20 years (HR = 4.64; P < .001). Conclusion In our series of BRCA carriers, we detected a relatively large effect on BC risk with a level of radiation exposure that is at least an order of magnitude lower than in previously studied medical radiation–exposed cohorts. Although part of this increase may be attributable to recall bias, the observed patterns of risk in terms of age at exposure and attained age are consistent with those found in previous studies. If confirmed, the results have important implications for the use of x-ray imaging in young BRCA1/2 carriers.

Published
2006
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6. Pregnancies, breast-feeding, and breast cancer risk in the International BRCA1/2 Carrier Cohort Study (IBCCS)

Author

Catherine Noguès, Nadine Andrieu, Susan Peock, Flora E. van Leeuwen, Matti A. Rookus, Fiona Douglas, Gareth Evans, Edith Olah, Richard M. Brohet, Brita Arver, David E. Goldgar, Javier Benitez, Irma Kluijt, Diana Eccles, Antonis C. Antoniou, Douglas F. Easton, Agnès Chompret, Jenny Chang-Claude, Marion Gauthier-Villars, Méthodologie statistique et épidémiologie génétique des maladies multifactorielles, Institut National de la Santé et de la Recherche Médicale (INSERM), Service de biostatistique (IC10213), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), International Agency for Cancer Research (IACR), Genetic Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge [UK] (CAM), Departments of Epidemiology and Molecular Pathology, The Netherlands Cancer Institute, Manchester regional genetics service, Manchester regional genetics service, Wessex clinical genetics service, Northern clinical genetics service, Laboratoire d'Oncogénétique, CRLCC René Huguenin, Service d'oncogénétique, Institut Curie [Paris], Département de médecine oncologique [Gustave Roussy], Institut Gustave Roussy (IGR), Departemento Genetica Humana, Centro Nacional Investigaciones Oncologicas, Radiumhemmet, Karolinska University Hospital [Stockholm], National Institute of Oncology, Division of Clinical Epidemiology, German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ), EMBRACE, GENEPSO, GEO-HEBON, IBCCS Collaborators' Group, and Andrieu, Nadine

Subjects
Cancer Research, Time Factors, MESH: Pregnan, International Cooperation, Genes, BRCA2, Genes, BRCA1, Cohort Studies, 0302 clinical medicine, Pregnancy, Surveys and Questionnaires, skin and connective tissue diseases, MESH: Cohort Studies, MESH: Heterozygote, 0303 health sciences, education.field_of_study, MESH: Middle Aged, Age Factors, MESH: Genetic Predisposition to Disease, Middle Aged, 3. Good health, Europe, Parity, Breast Feeding, Oncology, 030220 oncology & carcinogenesis, MESH: Breast Feeding, Cohort, Female, MESH: Abortion, Induced, Pregnancy Complications, Neoplastic, Cohort study, Adult, medicine.medical_specialty, Heterozygote, MESH: Mutation, Population, Breast Neoplasms, [SDV.CAN]Life Sciences [q-bio]/Cancer, Article, 03 medical and health sciences, Breast cancer, [SDV.CAN] Life Sciences [q-bio]/Cancer, medicine, Humans, Genetic Predisposition to Disease, Risk factor, education, 030304 developmental biology, Proportional Hazards Models, Retrospective Studies, Gynecology, MESH: Age Factors, MESH: Humans, business.industry, MESH: Parity, Retrospective cohort study, Abortion, Induced, MESH: Adult, medicine.disease, MESH: International Cooperation, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Mutation, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, MESH: Europe, business, Breast feeding, MESH: Female, MESH: Genes, BRCA1, MESH: Breast Neoplasms, MESH: Genes, BRCA2
Abstract

BACKGROUND: Multiparity, young age at first childbirth, and breast-feeding are associated with a reduced risk of breast cancer in the general population. The breast cancer predisposition gene, BRCA1, regulates normal cell differentiation. Because mammary gland cells divide and differentiate during pregnancy, reproductive factors may influence breast cancer risk in BRCA1/2 mutation carriers differently than they do in noncarriers. METHODS: We performed a retrospective cohort study of 1601 women in the International BRCA1/2 Carrier Cohort Study cohort, all of whom carried a mutation in BRCA1 or BRCA2. Information on reproductive factors was obtained from a questionnaire. At the time of interview 853 subjects were classified with breast cancer. Data were analyzed by using a weighted cohort approach. All statistical tests were two-sided. RESULTS: There was no statistically significant difference in the risk of breast cancer between parous and nulliparous women. Among parous women, an increasing number of full-term pregnancies was associated with a statistically significant decrease in the risk of breast cancer (Ptrend = .008); risk was reduced by 14% (95% confidence interval [CI] = 6% to 22%) for each additional birth. This association was the same for carriers of mutations in either BRCA1 or BRCA2 and was restricted to women older than 40 years. In BRCA2 mutation carriers, first childbirth at later ages was associated with an increased risk of breast cancer compared with first childbirth before age 20 years (20-24 years, hazard ratio [HR] = 2.33 [95% CI = 0.93 to 5.83]; 25-29 years, HR = 2.68 [95% CI = 1.02 to 7.07]; > or = 30 years, HR = 1.97 [95% CI = 0.67 to 5.81]), whereas in BRCA1 mutation carriers, first childbirth at age 30 years or later was associated with a reduced risk of breast cancer compared with first childbirth before age 20 years (HR = 0.58 [95% CI = 0.36 to 0.94]). Neither history of interrupted pregnancies (induced abortions or miscarriage) nor history of breast-feeding was statistically significantly associated with the risk of breast cancer. CONCLUSIONS: BRCA1 and BRCA2 mutation carriers older than 40 years show a similar reduction in breast cancer risk with increasing parity as non-carriers.

Published
2006
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