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5. Alcohol, tobacco and breast cancer--collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease

Author

Peterson, B., Ontiveros, P., Yu, M. C., Heath, C. W., Bergkvist, L., Baines, C. J., Malone, K., Magnusson, C., Lubin, F., Kungu, A., Kay, C., Pike, M., Siskind, V., Virutamasen, P., Hermon, C., Brêmond, A., Lacaya, L. B., Bain, C., Calle, E. E., Aristizabal, N., Gatei, D., Ngelangel, C. A., Bull, D., Fentiman, I. S., Leske, M. C., Hannaford, P., Pike, M. C., Viladiu, P., Wang, D. Y., Peto, J., White, E., Weinstein, A. L., Theetranont, C., Fraser, G., La Vecchia, C., Martinez, L., Evstifeeva, T., Holck, S., Jin, F., Shearman, R., Nasca, P. C., Wang, Q. S., Stanford, J. L., Chilvers, C. E.D., Tulinius, H., Bishop, T., Coldman, A. J., Salazar, S. B., Gallagher, R. P., Peto, R., Reeves, G., Hiatt, R. A., Kunde, D., Boyle, P., Kenya, P., Molina, R., Salas, O., Negri, E., Liff, J. M., Primic-Zakelj, M., Lee, N., Doll, R., Anderson, K., Schairer, C., Band, P., Goodill, A., Goldbohm, R. A., Katsouyanni, K., Hu, J., Mao, Y., Noonan, E. A., Hislop, T. G., Meirik, O., Cuadros, A., Clavel, F., Ursin, G., Boosiri, B., Lansac, J., Schofield, F., Renaud, R., Kosmelj, K., Kolonel, L. M., Hulka, B., Berry, G., Daling, J. R., Jones, L., Mati, J. G., Hulka, B. S., McCredie, M., Spears, G. F.S., Trichopoulou, A., Schuman, L., Farley, T. M.M., Ravnihar, B., Wei, H. Y., Key, T., Skegg, D. C.G., Lewis, C., Bernstein, L., Miller, A. B., Hanson, R. L., Ross, R. K., Martin, N., Rohan, T., Collins, R., Yuan, J. M., Colditz, G., Gao, Y. T., MacLennan, R., Segala, C., Weiss, N. S., Cooper Booth, J., Andrieu, N., Banks, E., Richardson, S., van Leeuwen, F. E., Newcomb, P., Gammon, M. D., Wongsrichanalai, C., Friedman, G. D., Szklo, M., Baens, J., van den Brandt, P. A., Alexander, F. E., Wilson, H. G., Spirtas, R., Tajima, K., Gerber, M., Franceschi, S., Stare, J., Ron, E., Jelihovsky, T., Mabuchi, K., Piana, L., Wall, C., Schoenberg, J. A., Koetsawang, S., Apelo, R. A., Marchbanks, P., Stewart, W., Van Leeuven, M., Jimakorn, P., Beeson, W. L., Pardthaisong, T., Tryggvadottir, L., Zheng, W., Adami, H. O., Coates, R. J., Palet, A., Wingo, P. A., Thomas, D. B., Thomas, D., Enger, S., Trichopoulos, D., Chutivongse, S., Bulbrook, R. D., Rosero-Bixby, L., Gajalakshmi, V., de la Cruz, J. R., Hopper, J. L., Muller, A., Zhiheng, C., Beral, V., Hamajima, N., Ewertz, M., Varma, A. O., Nomura, A. M.Y., Rookus, M. A., Lee, H. P., Ebeling, K., Cuzick, J., Yang, P., Cuevas, H. R., Peterson, H. B., Izquierdo, A., Brinton, L. A., Nishan, P., Clarke, E. A., Hayward, J. L., Crossley, B., Yun, T., Kalache, A., Moller, T. R., Hutchinson, W. B., Green, J., Marubini, E., Hoover, R., Wax, Y., Modan, B., Ory, H. W., Duffy, S. W., Ranstam, J., Olsson, H., Lund, E., Gairard, B., Ferraroni, M., Paganini-Hill, A., Appleby, P., Shu, X. O., Vessey, M., Haile, R. W., Dabancens, A., Folsom, A. R., Langston, N., Talamini, R., Skegg, D., Neil, A., Chang-Claude, J., Bachelot, A., McMichael, A. J., Javier, B., Persson, I., Paul, C., Mahoney, M. C., Hirose, K., Rachawat, D., De Sanjosé, S., Longnecker, M. P., Johnson, K. C., Morabia, A., Preston, D., Levi, F., Silpisornkosol, S., Stalsberg, H., McPherson, K., Yeates, D., Lê, M. G., Chantarakul, N., Clavel-Chapelon, F., Secretariat, Cancer Research UK Epidemiology Unit, Beral V, Hamajima N, Hirose K, Rohan T, Calle EE, Heath CW, Coates RJ, Liff JM, Talamini R, Chantarakul N, Koetsawang S, Rachawat D, Morabia A, Schuman L, Stewart W, Szklo M, Bain C, Schofield F, Siskind V, Band P, Coldman AJ, Gallagher RP, Hislop TG, Yang P, Kolonel LM, Nomura AMY, Hu J, Johnson KC, Mao Y, De Sanjose S, Lee N, Marchbanks P, Ory HW, Peterson HB, Wilson HG, Wingo PA, Ebeling K, Kunde D, Nishan P, Hopper JL, Colditz G, Gajalakshmi V, Martin N, Pardthaisong T, Solpisornkosol S, Theetranont C, Boosiri B, Chutivongse S, Jimakorn P, Virutamasen P, Wongsrichanalai C, Ewertz M, Adami HO, Bergkvist L, Magnusson C, Persson I, Chang-Claude J, Paul C, Skegg DCG, Spears GFS, Boyle P, Evstifeeva T, Daling JR, Hutchinson WB, Malone K, Noonan EA, Stanford JL, Thomas DB, Weiss NS, White E, Andrieu N, Bremond A, Clavel F, Gairard B, Lansac J, Piana L, Renaud R, Izquierdo A, Viladiu P, Cuevas HR, Ontiveros P, Palet A, Salazar SB, Arsitizabal N, Cuadros A, Tryggvadottir L, Tulinius H, Bachelot A, Le MG, Peto J, Franceschi S, Lubin F, Modan B, Ron E, Wax Y, Friedman GD, Hiatt RA, Levi F, Bishop T, Kosmelj K, Primic-Zakelj M, Ravnihar B, Stare J, Beeson WL, Fraser G, Bulbrook RD, Cuzick J, Duffy SW, Fentiman IS, Hayward JL, Wang DY, McMichael AJ, McPherson K, Hanson RL, Leske MC, Mahoney MC, Nasca PC, Varma AO, Weinstein AL, Moller TR, Olsson H, Ranstam J, Goldbohm RA, van den Brandt PA, Apelo RA, Baens J, de la Cruz JR, Javier B, Lacaya LB, Ngelangel CA, La Vecchia C, Negri E, Marubini E, Ferraroni M, Gerber M, Richardson S, Segala C, Gatei D, Kenya P, Kungu A, Mati JG, Brinton LA, Hoover R, Schairer C, Spirtas R, Lee HP, Rookus MA, van Leeuwen FE, Schoenberg JA, McCredie M, Gammon MD, Clarke EA, Jones L, Neil A, Vessey M, Yeates D, Appleby P, Banks E, Bull D, Crossley B, Goodill A, Green J, Hermon C, Key T, Langston N, Lewis C, Reeves G, Collins R, Doll R, Peto R, Mabuchi K, Preston D, Hannaford P, Kay C, Rosero-Bixby L, Gao YT, Jin F, Yuan JM, Wei HY, Yun T, Zhiheng C, Berry G, Cooper Booth J, Jelihovsky T, MacLennan R, Shearman R, Wang QS, Baines CJ, Miller AB, Wall C, Lund E, Stalsberg H, Shu XO, Zheng W, Katsouyanni K, Trichopoulou A, Trichopoulos D, Dabancens A, Martinez L, Molina R, Salas O, Alexander XE, Anderson K, Folsom AR, Hulka BS, Bernstein L, Enger S, Haile RW, Paganini-Hill A, Pike MC, Ross RK, Ursin G, Yu MC, Longnecker MP, Newcomb P, Kalache A, Farley TMM, Holck S, Meirik O, and Universitat de Barcelona

Subjects
Cancer Research, medicine.medical_specialty, Epidemiology, Dones, Alcohol, tobacco, smoking, Càncer de mama, chemistry.chemical_compound, Breast cancer, Hàbit de fumar, breast cancer, Tabac, Tobacco, [SDV.SPEE] Life Sciences [q-bio]/Public Health and Epidemiology, medicine, Women, Gynecology, collaborative reanalysis, Obstetrics, business.industry, alcohol, Confounding, Smoking, medicine.disease, Tobbacco habit, Oncology, chemistry, Drinking of alcoholic beverages, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Meta-analysis, Relative risk, Consum d'alcohol, Risk assessment, business, Developed country
Abstract

COLLABORATORS (in alphabetical order of institution, study name, or location) Aichi Cancer Research Institute, Nagoya, Japan: N Hamajima, K Hirose, K Tajima; Albert Einstein College of Medicine, NY, USA: T Rohan; American Cancer Society, GA, USA: EE Calle, CW Jr Heath; Atlanta, Emory University, GA, USA: RJ Coates, JM Liff; Aviano Cancer Center, Pordenone, Italy: R Talamini; Mahidol University, Bangkok, Thailand: N Chantarakul, S Koetsawang, D Rachawat; Breast Tumor Collaborative Study, Johns Hopkins University, MD, USA: A Morabia, L Schuman, W Stewart, M Szklo; University of Queensland, Brisbane, Australia: C Bain, F Schofield, V Siskind; British Columbia Cancer Agency, BC, Canada: P Band, AJ Coldman, RP Gallagher, TG Hislop, P Yang; Cancer Research Center, University of Hawaii, Hawaii, USA: LM Kolonel, AMY Nomura; Canadian Cancer Registries Epidemiology Research Group, Canada: J Hu, KC Johnson, Y Mao; Catalán Institut of Oncology, Barcelona, Spain: S De Sanjosé; Centers for Disease Control & Prevention, GA, USA: N Lee, P Marchbanks, HW Ory, HB Peterson, HG Wilson, PA Wingo; Central Institute of Cancer Research, Berlin, Germany: K Ebeling, D Kunde, P Nishan; Centre for Genetic Epidemiology, University of Melbourne, Melbourne, Australia: JL Hopper; Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, MA, USA: G Colditz for Nurses' Health Study Research Group; Chennai Cancer Institute, Madras, India: V Gajalakshmi; Chiang Mai University, Chiang Mai, Thailand: N Martin, T Pardthaisong, S Silpisornkosol, C Theetranont; Chulalongkorn University, Bangkok, Thailand: B Boosiri, S Chutivongse, P Jimakorn, P Virutamasen, C Wongsrichanalai; Danish Cancer Society, Aalborg, Denmark: M Ewertz; Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden: HO Adami, L Bergkvist, C Magnusson, I Persson; Deutsches Krebsforschungszentrum, Heidelberg, Germany: J Chang-Claude; University of Otago, Dunedin, New Zealand: C Paul, DCG Skegg, GFS Spears; European Institute of Oncology, Milan, Italy: P Boyle, T Evstifeeva; Fred Hutchinson Cancer Research Center, WA, USA: JR Daling, WB Hutchinson, K Malone, EA Noonan, JL Stanford, DB Thomas, NS Weiss, E White; French Multicentre Breast Study, INSERM, Villejuif, France: N Andrieu, A Brêmond, F Clavel, B Gairard, J Lansac, L Piana, R Renaud; Girona Cancer Registry, Girona, Spain: A Izquierdo, P Viladiu; Hospital General de Mexico, Mexico City, Mexico: HR Cuevas, P Ontiveros, A Palet, SB Salazar; Hospital Universitario, Cali, Colombia: N Aristizabal, A Cuadros; Icelandic Cancer Society, Reykjavik, Iceland: L Tryggvadottir, H Tulinius; INSERM, Institut Gustave-Roussey, Villejuif, France: A Bachelot, MG Lê; Institute of Cancer Research, Sutton and London School of Hygiene and Tropical Medicine, UK: J Peto; International Agency for Research in Cancer, Lyon, France: S Franceschi; Israel Chaim Sheba Medical Centre, Tel-Hashomer, Israel: F Lubin, B Modan, E Ron, Y Wax; Kaiser Permanente, CA, USA: GD Friedman, RA Hiatt; Institut universitaire de medecine sociale et preventive, Lausanne, Switzerland: F Levi; Cancer Research UK Genetic Epidemiology Laboratory, Leeds, UK: T Bishop; Institute of Oncology, Ljubljana, Slovenia: K Kosmelj, M Primic-Zakelj, B Ravnihar, J Stare; Loma Linda University, CA, USA: WL Beeson, G Fraser; Cancer Research UK Department of Mathematics, Statistics & Epidemiology, London: RD Bulbrook, J Cuzick, SW Duffy, IS Fentiman, JL Hayward, DY Wang; London School of Hygiene & Tropical Medicine, London, UK: AJ McMichael, K McPherson; Long Island Breast Cancer Study, NY, USA: RL Hanson, MC Leske, MC Mahoney, PC Nasca, AO Varma, AL Weinstein; University Hospital, Lund, Sweden: TR Moller, H Olsson, J Ranstam; Maastricht University, Maastricht, The Netherlands: RA Goldbohm, PA van den Brandt; University of Philippines, Manila, Philippines: RA Apelo, J Baens, JR de la Cruz, B Javier, LB Lacaya, CA Ngelangel; Istituto ‘Mario Negri', Milan, Italy: C La Vecchia, E Negri; Istituto Nazionale Tumori, Divisione di Statistica Medica e Biometria, Milan, Italy: E Marubini; Istituto di Statistica Medica e Biometria, Milan, Italy: M Ferraroni; Montpellier Cancer Centre & INSERM, Montpellier, France: M Gerber, S Richardson, C Segala; Nairobi Centre for Research in Reproduction, Nairobi, Kenya: D Gatei, P Kenya, A Kungu, JG Mati; National Cancer Institute, MD, USA: LA Brinton, R Hoover, C Schairer; National Institute of Child Health & Human Development, MD, USA: R Spirtas; National University of Singapore, Singapore: HP Lee; The Netherlands Cancer Institute, Amsterdam, The Netherlands: MA Rookus, FE van Leeuwen for the Netherlands Oral Contraceptives and Breast Cancer Study Group; New Jersey State Department of Health, NJ, USA: JA Schoenberg; New South Wales Cancer Council, Sydney, Australia: M McCredie; Columbia University School of Public Health, NY, USA: MD Gammon; Ontario Cancer Treatment & Research Foundation, Ontario, Canada: EA Clarke; Department of Public Health & Primary Care, Oxford, UK: L Jones, A Neil, M Vessey, D Yeates; Cancer Research UK Epidemiology Unit, Oxford, UK (Secretariat): P Appleby, E Banks, V Beral, D Bull, B Crossley, A Goodill, J Green, C Hermon, T Key, N Langston, C Lewis, G Reeves; Cancer Research UK/MRC/BHF Clinical Trial Service Unit & Epidemiological Studies Unit, Oxford, UK: R Collins, R Doll, R Peto; Radiation Effects Research Foundation, Hiroshima, Japan: K Mabuchi, D Preston; Royal College of General Practitioners Oral Contraception Study, London, UK: P Hannaford, C Kay; University of Costa Rica, San Jose, Costa Rica: L Rosero-Bixby; Shanghai Cancer Institute, Shanghai, China: YT Gao, F Jin, J-M Yuan; Shanghai Institute of Planned Parenthood Research, Shanghai, China: HY Wei, T Yun, C Zhiheng; Department of Public Health, Sydney, Australia: G Berry, J Cooper Booth, T Jelihovsky, R MacLennan, R Shearman; Tianjin Cancer Institute, Tianjin, China: Q-S Wang; Department of Public Health Sciences, Toronto, Canada: CJ Baines, AB Miller, C Wall; Tromso University, Tromso, Norway: E Lund, H Stalsberg; Vanderbilt University, TN, USA: XO Shu, W Zheng; University of Athens Medical School, Athens, Greece: K Katsouyanni, A Trichopoulou, D Trichopoulos; University of Chile, Santiago, Chile: A Dabancens, L Martinez, R Molina, O Salas; University of Edinburgh, Edinburgh, UK: FE Alexander; University of Minnesota School of Public Health, MN, USA: K Anderson, AR Folsom on behalf of the Iowa Women's Health Study; University of North Carolina at Chapel Hill, School of Public Health, NC, USA: BS Hulka; University of Nottingham, Nottingham, UK: CED Chilvers; University of Southern California, LA, USA: L Bernstein, S Enger, RW Haile, A Paganini-Hill, MC Pike, RK Ross, G Ursin, MC Yu; University of Wisconsin Comprehensive Cancer Center, WI, USA: MP Longnecker, P Newcomb for the 4 State Study; Vasteras, Sweden: L Bergkvist; World Health Organisation, Geneva, Switzerland: A Kalache; World Health Organisation, UNDP/UNFPA/WHO/World Bank Special Programme of Research, Development and Research Training in Human Reproduction, Geneva, Switzerland: TMM Farley, S Holck, O Meirik. Analysis and writing committee: Beral V, Bull D, Doll R, Peto R, Reeves G Steering committee: Skegg D (Chairman), Colditz G, Hulka B, La Vecchia C, Magnusson C, Muller A, Peterson B, Pike M, Thomas D, Van Leeuven M.; International audience; Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58,515 women with invasive breast cancer and 95,067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19-1.45, P/=45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P

Published
2002
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6. Menarche, menopause, and breast cancer risk: individual participant meta-analysis, including 118 964 women with breast cancer from 117 epidemiological studies

Author

Beral, V, Bull, D, Pirie, K, Reeves, G, Peto, R, Skegg, D, LaVecchia, C, Magnusson, C, Pike, MC, Thomas, D, Hamajima, N, Hirose, K, Tajima, K, Rohan, T, Friedenreich, CM, Calle, EE, Gapstur, SM, Patel, AV, Coates, RJ, Liff, JM, Talamini, R, Chantarakul, N, Koetsawang, S, Rachawat, D, Marcou, Y, Kakouri, E, Duffy, SW, Morabia, A, Schuman, L, Stewart, W, Szklo, M, Coogan, PF, Palmer, JR, Rosenberg, L, Band, P, Coldman, AJ, Gallagher, RP, Hislop, TG, Yang, P, Cummings, SR, Canfell, K, Sitas, F, Chao, P, Lissowska, J, Horn-Ross, PL, John, EM, Kolonel, LM, Nomura, AMY, Ghiasvand, R, Hu, J, Johnson, KC, Mao, Y, Callaghan, K, Crossley, B, Goodill, A, Green, J, Hermon, C, Key, T, Lindgard, I, Liu, B, Collins, R, Doll, R, Bishop, T, Fentiman, IS, De Sanjose, S, Gonzaler, CA, Lee, N, Marchbanks, P, Ory, HW, Peterson, HB, Wingo, P, Ebeling, K, Kunde, D, Nishan, P, Hopper, JL, Eliassen, H, Gajalakshmi, V, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Neugut, A, Santella, R, Baines, CJ, Kreiger, N, Miller, AB, Wall, C, Tjonneland, A, Jorgensen, T, Stahlberg, C, Pedersen, AT, Flesch-Janys, D, Hakansson, N, Cauley, J, Heuch, I, Adami, HO, Persson, I, Weiderpass, E, Chang-Claude, J, Kaaks, R, McCredie, M, Paul, C, Skegg, DCG, Spears, GFS, Iwasaki, M, Tsugane, S, Anderson, G, Daling, JR, Hampton, J, Hutchinson, WB, Li, CI, Malone, K, Mandelson, M, Newcomb, P, Noonan, EA, Ray, RM, Stanford, JL, Tang, MTC, Thomas, DB, Weiss, NS, White, E, Izquierdo, A, Viladiu, P, Fourkala, EO, Jacobs, I, Menon, U, Ryan, A, Cuevas, HR, Ontiveros, P, Palet, A, Salazar, SB, Aristizabal, N, Cuadros, A, Tryggvadottir, L, Tulinius, H, Riboli, E, Andrieu, N, Bachelot, A, Le, MG, Bremond, A, Gairard, B, Lansac, J, Piana, L, Renaud, R, Clavel-Chapelon, F, Fournier, A, Touillaud, M, Mesrine, S, Chabbert-Buffet, N, Boutron-Ruault, MC, Wolk, A, Torres-Mejia, G, Franceschi, S, Romieu, I, Boyle, P, Lubin, F, Modan, B, Ron, E, Wax, Y, Friedman, GD, Hiatt, RA, Levi, F, Kosmelj, K, Primic-Zakelj, M, Ravnihar, B, Stare, J, Ekbom, A, Erlandsson, G, Beeson, WL, Fraser, G, Peto, J, Hanson, RL, Leske, MC, Mahoney, MC, Nasca, PC, Varma, AO, Weinstein, AL, Hartman, ML, Olsson, H, Goldbohm, RA, van den Brandt, PA, Palli, D, Teitelbaum, S, Apelo, RA, Baens, J, de la Cruz, JR, Javier, B, Lacaya, LB, Ngelangel, CA, La Vecchia, C, Negri, E, Marubini, E, Ferraroni, M, Gerber, M, Richardson, S, Segala, C, Gatei, D, Kenya, P, Kungu, A, Mati, JG, Brinton, LA, Freedman, M, Hoover, R, Schairer, C, Ziegler, R, Banks, E, Spirtas, R, Lee, HP, Rookus, MA, van Leeuwen, FE, Schoenberg, JA, Graff-Iversen, S, Selmer, R, Jones, L, McPherson, K, Neil, A, Vessey, M, Yeates, D, Mabuchi, K, Preston, D, Hannaford, P, Kay, C, McCann, SE, Rosero-Bixby, L, Gao, YT, Jin, F, Yuan, J-M, Wei, HY, Yun, T, Zhiheng, C, Berry, G, Booth, JC, Jelihovsky, T, MacLennan, R, Shearman, R, Hadjisavvas, A, Kyriacou, K, Loisidou, M, Zhou, X, Wang, Q-S, Kawai, M, Minami, Y, Tsuji, I, Lund, E, Kumle, M, Stalsberg, H, Shu, XO, Zheng, W, Monninkhof, EM, Onland-Moret, NC, Peeters, PHM, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Tzonou, A, Baltzell, KA, Dabancens, A, Martinez, L, Molina, R, Salas, O, Alexander, FE, Anderson, K, Folsom, AR, Gammon, MD, Hulka, BS, Millikan, R, Chilvers, CED, Lumachi, F, Bain, C, Schofield, F, Siskind, V, Rebbeck, TR, Bernstein, LR, Enger, S, Haile, RW, Paganini-Hill, A, Ross, RK, Ursin, G, Wu, AH, Yu, MC, Ewertz, DM, Clarke, EA, Bergkvist, L, Anderson, GL, Gass, M, O'Sullivan, MJ, Kalache, A, Farley, TMM, Holck, S, Meirik, O, Fukao, A, Factors, CGH, Grp, SHNHSIIIR, Epidemiologie, RS: CAPHRI School for Public Health and Primary Care, RS: GROW - School for Oncology and Reproduction, RS: GROW - R1 - Prevention, RS: CAPHRI - R5 - Optimising Patient Care, and Collaborative Group on Hormonal Factors in Breast Cancer

Subjects
Aging, Breast cancer, Risk factors, Menopause, Menarche, cancer, malignancy, Ethnic origin, Disease, 0302 clinical medicine, Breast cancer, Risk Factors, Neoplasms, Receptors, Epidemiology, 80 and over, 030212 general & internal medicine, skin and connective tissue diseases, Aged, 80 and over, Patient, Obstetrics, Reproduction, Smoking, Age Factors, Middle Aged, Reproducibility, 3. Good health, Menopause, Receptors, Estrogen, Oncology, 030220 oncology & carcinogenesis, Menarche, Hormonal therapy, Female, epidemiology, Cancer Type - Breast Cancer, history, Adult, Risk, trends, medicine.medical_specialty, Design, Neoplasms, Hormone-Dependent, Requiring prolonged observation, Hormone Replacement Therapy, Oncology and Carcinogenesis, Breast Neoplasms, and over, Validity, methods, 03 medical and health sciences, Age, Clinical Research, Breast Cancer, medicine, Humans, cancer, Neoplasm Invasiveness, Women, Oncology & Carcinogenesis, Hormone-Dependent, breast, Aged, Gynecology, Collaborative Group on Hormonal Factors in Breast Cancer, therapy, business.industry, Contraception/Reproduction, Research, Estrogens, Etiology - Resources and Infrastructure, medicine.disease, Estrogen, Good Health and Well Being, cessation, Premenopause, Risk factors, Relative risk, Recall, business, malignancy, Meta-Analysis
Abstract

Background Menarche and menopause mark the onset and cessation, respectively, of ovarian activity associated with reproduction, and affect breast cancer risk. Our aim was to assess the strengths of their effects and determine whether they depend on characteristics of the tumours or the affected women.Methods Individual data from 117 epidemiological studies, including 118 964 women with invasive breast cancer and 306 091 without the disease, none of whom had used menopausal hormone therapy, were included in the analyses. We calculated adjusted relative risks (RRs) associated with menarche and menopause for breast cancer overall, and by tumour histology and by oestrogen receptor expression.Findings Breast cancer risk increased by a factor of 1.050 (95% CI 1.044-1.057; p < 0.0001) for every year younger at menarche, and independently by a smaller amount (1.029, 1.025-1.032; p < 0.0001), for every year older at menopause. Premenopausal women had a greater risk of breast cancer than postmenopausal women of an identical age (RR at age 45-54 years 1.43, 1.33-1.52, p < 0.001). All three of these associations were attenuated by increasing adiposity among postmenopausal women, but did not vary materially by women's year of birth, ethnic origin, childbearing history, smoking, alcohol consumption, or hormonal contraceptive use. All three associations were stronger for lobular than for ductal tumours (p < 0.006 for each comparison). The effect of menopause in women of an identical age and trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p < 0.01 for both comparisons).Interpretation The effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women's total number of reproductive years. Endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours.Funding Cancer Research UK.

Published
2012
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7. Menarche, menopause, and breast cancer risk: individual participant meta-analysis, including 118 964 women with breast cancer from 117 epidemiological studies

Author

Beral, V. Bull, D. Pirie, K. Reeves, G. Peto, R. and Skegg, D. LaVecchia, C. Magnusson, C. Pike, M. C. and Thomas, D. Hamajima, N. Hirose, K. Tajima, K. Rohan, T. and Friedenreich, C. M. Calle, E. E. Gapstur, S. M. Patel, A. V. Coates, R. J. Liff, J. M. Talamini, R. and Chantarakul, N. Koetsawang, S. Rachawat, D. Marcou, Y. and Kakouri, E. Duffy, S. W. Morabia, A. Schuman, L. and Stewart, W. Szklo, M. Coogan, P. F. Palmer, J. R. and Rosenberg, L. Band, P. Coldman, A. J. Gallagher, R. P. and Hislop, T. G. Yang, P. Cummings, S. R. Canfell, K. and Sitas, F. Chao, P. Lissowska, J. Horn-Ross, P. L. John, E. M. Kolonel, L. M. Nomura, A. M. Y. Ghiasvand, R. Hu, J. Johnson, K. C. Mao, Y. Callaghan, K. Crossley, B. and Goodill, A. Green, J. Hermon, C. Key, T. Lindgard, I. and Liu, B. Collins, R. Doll, R. Bishop, T. Fentiman, I. S. De Sanjose, S. Gonzaler, C. A. Lee, N. Marchbanks, P. and Ory, H. W. Peterson, H. B. Wingo, P. Ebeling, K. and Kunde, D. Nishan, P. Hopper, J. L. Eliassen, H. and Gajalakshmi, V. Martin, N. Pardthaisong, T. Silpisornkosol, S. Theetranont, C. Boosiri, B. Chutivongse, S. Jimakorn, P. Virutamasen, P. Wongsrichanalai, C. Neugut, A. and Santella, R. Baines, C. J. Kreiger, N. Miller, A. B. and Wall, C. Tjonneland, A. Jorgensen, T. Stahlberg, C. and Pedersen, A. Tonnes Flesch-Janys, D. Hakansson, N. Cauley, J. Heuch, I. Adami, H. O. Persson, I. Weiderpass, E. and Chang-Claude, J. Kaaks, R. McCredie, M. Paul, C. Spears, G. F. S. Iwasaki, M. Tsugane, S. Anderson, G. Daling, J. R. Hampton, J. Hutchinson, W. B. Li, C. I. Malone, K. and Mandelson, M. Newcomb, P. Noonan, E. A. Ray, R. M. and Stanford, J. L. Tang, M. T. C. Weiss, N. S. White, E. and Izquierdo, A. Viladiu, P. Fourkala, E. O. Jacobs, I. and Menon, U. Ryan, A. Cuevas, H. R. Ontiveros, P. Palet, A. and Salazar, S. B. Aristizabal, N. Cuadros, A. and Tryggvadottir, L. Tulinius, H. Riboli, E. Andrieu, N. and Bachelot, A. Le, M. G. Bremond, A. Gairard, B. Lansac, J. Piana, L. Renaud, R. Clavel-Chapelon, F. Fournier, A. and Touillaud, M. Mesrine, S. Chabbert-Buffet, N. and Boutron-Ruault, M. C. Wolk, A. Torres-Mejia, G. Franceschi, S. Romieu, I. Boyle, P. Lubin, F. Modan, B. Ron, E. and Wax, Y. Friedman, G. D. Hiatt, R. A. Levi, F. and Kosmelj, K. Primic-Zakelj, M. Ravnihar, B. Stare, J. and Ekbom, A. Erlandsson, G. Beeson, W. L. Fraser, G. Peto, J. Hanson, R. L. Leske, M. C. Mahoney, M. C. Nasca, P. C. Varma, A. O. Weinstein, A. L. Hartman, M. L. Olsson, H. Goldbohm, R. A. van den Brandt, P. A. Palli, D. and Teitelbaum, S. Apelo, R. A. Baens, J. de la Cruz, J. R. and Javier, B. Lacaya, L. B. Ngelangel, C. A. La Vecchia, C. and Negri, E. Marubini, E. Ferraroni, M. Gerber, M. and Richardson, S. Segala, C. Gatei, D. Kenya, P. Kungu, A. and Mati, J. G. Brinton, L. A. Freedman, M. Hoover, R. and Schairer, C. Ziegler, R. Banks, E. Spirtas, R. Lee, H. P. Rookus, M. A. van Leeuwen, F. E. Schoenberg, J. A. and Graff-Iversen, S. Selmer, R. Jones, L. McPherson, K. and Neil, A. Vessey, M. Yeates, D. Mabuchi, K. Preston, D. and Hannaford, P. Kay, C. McCann, S. E. Rosero-Bixby, L. and Gao, Y. T. Jin, F. Yuan, J-M Wei, H. Y. Yun, T. and Zhiheng, C. Berry, G. Booth, J. Cooper Jelihovsky, T. and MacLennan, R. Shearman, R. Hadjisavvas, A. Kyriacou, K. and Loisidou, M. Zhou, X. Wang, Q-S Kawai, M. Minami, Y. and Tsuji, I. Lund, E. Kumle, M. Stalsberg, H. Shu, X. O. and Zheng, W. Monninkhof, E. M. Onland-Moret, N. C. Peeters, P. H. M. Katsouyanni, K. Trichopoulou, A. Trichopoulos, D. and Tzonou, A. Baltzell, K. A. Dabancens, A. Martinez, L. and Molina, R. Salas, O. Alexander, F. E. Anderson, K. and Folsom, A. R. Gammon, M. D. Hulka, B. S. Millikan, R. and Chilvers, C. E. D. Lumachi, F. Bain, C. Schofield, F. and Siskind, V. Rebbeck, T. R. Bernstein, L. R. Enger, S. and Haile, R. W. Paganini-Hill, A. Ross, R. K. Ursin, G. Wu, A. H. Yu, M. C. Ewertz, Denmark M. Clarke, E. A. and Bergkvist, L. Gass, M. O'Sullivan, M. J. Kalache, A. and Farley, T. M. M. Holck, S. Meirik, O. Fukao, A. and Collaborative Grp Hormonal Factors Collaborative Grp Hormonal Factors S Hankinson Nurses Hlth Study I II

Subjects
skin and connective tissue diseases
Abstract

Background Menarche and menopause mark the onset and cessation, respectively, of ovarian activity associated with reproduction, and affect breast cancer risk. Our aim was to assess the strengths of their effects and determine whether they depend on characteristics of the tumours or the affected women. Methods Individual data from 117 epidemiological studies, including 118 964 women with invasive breast cancer and 306 091 without the disease, none of whom had used menopausal hormone therapy, were included in the analyses. We calculated adjusted relative risks (RRs) associated with menarche and menopause for breast cancer overall, and by tumour histology and by oestrogen receptor expression. Findings Breast cancer risk increased by a factor of 1.050 (95% CI 1.044-1.057; p < 0.0001) for every year younger at menarche, and independently by a smaller amount (1.029, 1.025-1.032; p < 0.0001), for every year older at menopause. Premenopausal women had a greater risk of breast cancer than postmenopausal women of an identical age (RR at age 45-54 years 1.43, 1.33-1.52, p < 0.001). All three of these associations were attenuated by increasing adiposity among postmenopausal women, but did not vary materially by women’s year of birth, ethnic origin, childbearing history, smoking, alcohol consumption, or hormonal contraceptive use. All three associations were stronger for lobular than for ductal tumours (p < 0.006 for each comparison). The effect of menopause in women of an identical age and trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p < 0.01 for both comparisons). Interpretation The effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women’s total number of reproductive years. Endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours. Funding Cancer Research UK.

Published
2012

8. Alcohol, tobacco and breast cancer - collaborative reanalysis of individual data from 53 epidemiological studies, including 58515 women with breast cancer and 95067 women without the disease

Author

Beral, V Hamajima, N Hirose, K Rohan, T Calle, EE and Heath, CW Coates, RJ Liff, JM Talamini, R Chantarakul, N and Koetsawang, S Rachawat, D Morabia, A Schuman, L and Stewart, W Szklo, M Bain, C Schofield, F Siskind, V and Band, P Coldman, AJ Gallagher, RP Hislop, TG Yang, P and Kolonel, LM Nomura, AMY Hu, J Johnson, KC Mao, Y De Sanjose, S Lee, N Marchbanks, P Ory, HW Peterson, HB and Wilson, HG Wingo, PA Ebeling, K Kunde, D Nishan, P and Hopper, JL Colditz, G Gajalakshmi, V Martin, N and Pardthaisong, T Solpisornkosol, S Theetranont, C Boosiri, B and Chutivongse, S Jimakorn, P Virutamasen, P and Wongsrichanalai, C Ewertz, M Adami, HO Bergkvist, L and Magnusson, C Persson, I Chang-Claude, J Paul, C Skegg, DCG Spears, GFS Boyle, P Evstifeeva, T Daling, JR and Hutchinson, WB Malone, K Noonan, EA Stanford, JL Thomas, DB Weiss, NS White, E Andrieu, N Bremond, A Clavel, F Gairard, B Lansac, J Piana, L Renaud, R Izquierdo, A Viladiu, P Cuevas, HR Ontiveros, P Palet, A and Salazar, SB Arsitizabal, N Cuadros, A Tryggvadottir, L and Tulinius, H Bachelot, A Le, MG Peto, J Franceschi, S and Lubin, F Modan, B Ron, E Wax, Y Friedman, GD Hiatt, RA Levi, F Bishop, T Kosmelj, K Primic-Zakelj, M and Ravnihar, B Stare, J Beeson, WL Fraser, G Bulbrook, RD and Cuzick, J Duffy, SW Fentiman, IS Hayward, JL Wang, DY McMichael, AJ McPherson, K Hanson, RL Leske, MC and Mahoney, MC Nasca, PC Varma, AO Weinstein, AL Moller, TR and Olsson, H Ranstam, J Goldbohm, RA van den Brandt, PA and Apelo, RA Baens, J de la Cruz, JR Javier, B Lacaya, LB and Ngelangel, CA La Vecchia, C Negri, E Marubini, E and Ferraroni, M Gerber, M Richardson, S Segala, C Gatei, D and Kenya, P Kungu, A Mati, JG Brinton, LA Hoover, R and Schairer, C Spirtas, R Lee, HP Rookus, MA van Leeuwen, FE Schoenberg, JA McCredie, M Gammon, MD Clarke, EA and Jones, L Neil, A Vessey, M Yeates, D Appleby, P and Banks, E Bull, D Crossley, B Goodill, A Green, J and Hermon, C Key, T Langston, N Lewis, C Reeves, G and Collins, R Doll, R Peto, R Mabuchi, K Preston, D and Hannaford, P Kay, C Rosero-Bixby, L Gao, YT Jin, F and Yuan, JM Wei, HY Yun, T Zhiheng, C Berry, G Cooper Booth, J Jelihovsky, T MacLennan, R Shearman, R Wang, QS and Baines, CJ Miller, AB Wall, C Lund, E Stalsberg, H and Shu, XO Zheng, W Katsouyanni, K Trichopoulou, A and Trichopoulos, D Dabancens, A Martinez, L Molina, R and Salas, O Alexander, XE Anderson, K Folsom, AR Hulka, BS and Bernstein, L Enger, S Haile, RW Paganini-Hill, A and Pike, MC Ross, RK Ursin, G Yu, MC Longnecker, MP and Newcomb, P Bergkvist, L Kalache, A Farley, TMM Holck, S and Meirik, O Collaborative Group on Hormonal Factors in Breast Cancer

Abstract

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58515 women with invasive breast cancer and 95067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women’s age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19 - 1.45, P < 0.00001) for an intake of 35 - 44 g per day alcohol, and 1.46 (1.33 - 1.61, P < 0.00001) for greater than or equal to 45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P

Published
2002

9. Genome-wide association study identifies novel breast cancer susceptibility loci.

Author

Cox A., Farshid G., Fawcett S., Field M., Firgaira F., Fleming J., Forbes J., Friedlander M., Gaff C., Gardner M., Gattas M., George P., Gill G., Goldblatt J., Greening S., Haan E., Hart S., Humphrey E., Jenkins M., Kefford R., Kirk J., Kollias J., Kovalenko S., Lakhani S., Leary J., Lim J., Lindeman G., Lipton L., Lobb L., Maclurcan M., Marsh D., McKay M., Anne McLachlan S., Mitchell G., Newman B., O'Loughlin I., Osborne R., Peters L., Price M., Reeve J., Reeve T., Richards R., Rinehart G., Robinson B., Rudzki B., Salisbury E., Saunders C., Scott E., Seshadri R., Shelling A., Suthers G., Taylor D., Tennant C., Townshend S., Tyler J., Venter D., Visvader J., Walpole I., Ward R., Warner B., Warren G., Watson E., Williams R., Winship I., Bowtell D., Green A., DeFazio A., Gertig D., Webb P., Milne R., Young M.A., Harris M., Wilson J., Easton D.F., Pooley K.A., Dunning A.M., Pharoah P.D.P., Thompson D., Ballinger D.G., Struewing J.P., Morrison J., Field H., Luben R., Wareham N., Ahmed S., Healey C.S., Bowman R., Meyer K.B., Haiman C.A., Kolonel L.K., Henderson B.E., Le Marchand L., Brennan P., Sangrajrang S., Gaborieau V., Odefrey F., Shen C.-Y., Wu P.-E., Wang H.-C., Eccles D., Evans D.G., Peto J., Fletcher O., Johnson N., Seal S., Stratton M.R., Rahman N., Chenevix-Trench G., Bojesen S.E., Nordestgaard B.G., Axelsson C.K., Garcia-Closas M., Brinton L., Chanock S., Lissowska J., Peplonska B., Nevanlinna H., Fagerholm R., Eerola H., Kang D., Yoo K.-Y., Noh D.-Y., Ahn S.-H., Hunter D.J., Hankinson S.E., Cox D.G., Hall P., Wedren S., Liu J., Low Y.-L., Bogdanova N., Schurmann P., Dork T., Tollenaar R.A.E.M., Jacobi C.E., Devilee P., Klijn J.G.M., Sigurdson A.J., Doody M.M., Alexander B.H., Zhang J., Brock I.W., MacPherson G., Reed M.W.R., Couch F.J., Goode E.L., Olson J.E., Meijers-Heijboer H., Van Den Ouweland A., Uitterlinden A., Rivadeneira F., Milne R.L., Ribas G., Gonzalez-Neira A., Benitez J., Hopper J., McCredie M., Southey M., Giles G., Schroen C., Justenhoven C., Brauch H., Hamann U., Ko Y.-D., Spurdle A.B., Beesley J., Chen X., Mannermaa A., Kosma V.-M., Kataja V., Hartikainen J., Day N.E., Cox D.R., Ponder B.A.J., Luccarini C., Conroy D., Shah M., Munday H., Jordan C., Perkins B., West J., Redman K., Driver K., Aghmesheh M., Amor D., Andrews L., Antill Y., Armes J., Armitage S., Arnold L., Balleine R., Begley G., Beilby J., Bennett I., Bennett B., Berry G., Blackburn A., Brennan M., Brown M., Buckley M., Burke J., Butow P., Byron K., Callen D., Campbell I., Clarke C., Colley A., Cotton D., Cui J., Culling B., Cummings M., Dawson S.-J., Dixon J., Dobrovic A., Dudding T., Edkins T., Eisenbruch M., Cox A., Farshid G., Fawcett S., Field M., Firgaira F., Fleming J., Forbes J., Friedlander M., Gaff C., Gardner M., Gattas M., George P., Gill G., Goldblatt J., Greening S., Haan E., Hart S., Humphrey E., Jenkins M., Kefford R., Kirk J., Kollias J., Kovalenko S., Lakhani S., Leary J., Lim J., Lindeman G., Lipton L., Lobb L., Maclurcan M., Marsh D., McKay M., Anne McLachlan S., Mitchell G., Newman B., O'Loughlin I., Osborne R., Peters L., Price M., Reeve J., Reeve T., Richards R., Rinehart G., Robinson B., Rudzki B., Salisbury E., Saunders C., Scott E., Seshadri R., Shelling A., Suthers G., Taylor D., Tennant C., Townshend S., Tyler J., Venter D., Visvader J., Walpole I., Ward R., Warner B., Warren G., Watson E., Williams R., Winship I., Bowtell D., Green A., DeFazio A., Gertig D., Webb P., Milne R., Young M.A., Harris M., Wilson J., Easton D.F., Pooley K.A., Dunning A.M., Pharoah P.D.P., Thompson D., Ballinger D.G., Struewing J.P., Morrison J., Field H., Luben R., Wareham N., Ahmed S., Healey C.S., Bowman R., Meyer K.B., Haiman C.A., Kolonel L.K., Henderson B.E., Le Marchand L., Brennan P., Sangrajrang S., Gaborieau V., Odefrey F., Shen C.-Y., Wu P.-E., Wang H.-C., Eccles D., Evans D.G., Peto J., Fletcher O., Johnson N., Seal S., Stratton M.R., Rahman N., Chenevix-Trench G., Bojesen S.E., Nordestgaard B.G., Axelsson C.K., Garcia-Closas M., Brinton L., Chanock S., Lissowska J., Peplonska B., Nevanlinna H., Fagerholm R., Eerola H., Kang D., Yoo K.-Y., Noh D.-Y., Ahn S.-H., Hunter D.J., Hankinson S.E., Cox D.G., Hall P., Wedren S., Liu J., Low Y.-L., Bogdanova N., Schurmann P., Dork T., Tollenaar R.A.E.M., Jacobi C.E., Devilee P., Klijn J.G.M., Sigurdson A.J., Doody M.M., Alexander B.H., Zhang J., Brock I.W., MacPherson G., Reed M.W.R., Couch F.J., Goode E.L., Olson J.E., Meijers-Heijboer H., Van Den Ouweland A., Uitterlinden A., Rivadeneira F., Milne R.L., Ribas G., Gonzalez-Neira A., Benitez J., Hopper J., McCredie M., Southey M., Giles G., Schroen C., Justenhoven C., Brauch H., Hamann U., Ko Y.-D., Spurdle A.B., Beesley J., Chen X., Mannermaa A., Kosma V.-M., Kataja V., Hartikainen J., Day N.E., Cox D.R., Ponder B.A.J., Luccarini C., Conroy D., Shah M., Munday H., Jordan C., Perkins B., West J., Redman K., Driver K., Aghmesheh M., Amor D., Andrews L., Antill Y., Armes J., Armitage S., Arnold L., Balleine R., Begley G., Beilby J., Bennett I., Bennett B., Berry G., Blackburn A., Brennan M., Brown M., Buckley M., Burke J., Butow P., Byron K., Callen D., Campbell I., Clarke C., Colley A., Cotton D., Cui J., Culling B., Cummings M., Dawson S.-J., Dixon J., Dobrovic A., Dudding T., Edkins T., and Eisenbruch M.

Abstract

Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r2> 0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P < 10-7). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1). At the second stage, 1,792 SNPs were significant at the P < 0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach. ©2007 Nature Publishing Group.

Published
2007

10. Cytomegalovirus, Epstein-Barr virus and risk of breast cancer before age 40 years: a case-control study

Author

Richardson, AK, Cox, B, McCredie, M, Dite, GS, Chang, JH, Gertig, DM, Southey, MC, Giless, GG, Hopper, JL, Richardson, AK, Cox, B, McCredie, M, Dite, GS, Chang, JH, Gertig, DM, Southey, MC, Giless, GG, and Hopper, JL

Abstract

We investigated whether there is an association between cytomegalovirus (CMV) and Epstein-Barr virus (EBV) IgG levels and risk of breast cancer before age 40 years. CMV and EBV IgG levels were measured in stored plasma from 208 women with breast cancer and 169 controls who participated in the Australian Breast Cancer Family Study (ABCFS), a population-based case-control study. CMV and EBV IgG values were measured in units of optical density (OD). Cases and controls did not differ in seropositivity for CMV (59 and 57% respectively; P=0.8) or EBV (97 and 96% respectively; P=0.7). In seropositive women, mean IgG values were higher in cases than controls for CMV (1.20 vs 0.98 OD, P=0.005) but not for EBV (2.65 vs 2.57 OD, P=0.5). The adjusted odds ratios per OD unit were 1.46 (95% CI 1.06-2.03) for CMV IgG and 1.11 (0.93-1.33) for EBV IgG. The higher mean CMV IgG levels found in women with breast cancer could be the result of a more recent infection with CMV, and may mean that late exposure to CMV is a risk factor for breast cancer.

Published
2004

14. Alcohol, tobacco and breast cancer--collaborative reanalysis of individualdata from 53 epidemiological studies, including 58,515 women with breastcancer and 95,067 women without the disease.

Author

Hamajima, N, Hirose, K, Tajima, K, Rohan, T, Calle, EE, Heath CW, Jr, Coates, RJ, Liff, JM, Talamini, R, Chantarakul, N, Koetsawang, S, Rachawat, D, Morabia, A, Schuman, L, Stewart, W, Szklo, M, Bain, C, Schofield, F, Siskind, V, Band, P, Coldman, AJ, Gallagher, RP, Hislop, TG, Yang, P, Kolonel, LM, Nomura, AM, Hu, J, Johnson, KC, Mao, Y, De Sanjose, S, Lee, N, Marchbanks, P, Ory, HW, Peterson, HB, Wilson, HG, Wingo, PA, Ebeling, K, Kunde, D, Nishan, P, Hopper, JL, Colditz, G, Gajalanski, V, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Ewertz, M, Adami, HO, Bergkvist, L, Magnusson, C, Persson, I, Chang-Claude, J, Paul, C, Skegg, DC, Spears, GF, Boyle, P, Evstifeeva, T, Daling, JR, Hutchinson, WB, Malone, K, Noonan, EA, Stanford, JL, Thomas, DB, Weiss, NS, White, E, Andrieu, N, Bremond, A, Clavel, F, Gairard, B, Lansac, J, Piana, L, Renaud, R, Izquierdo, A, Viladiu, P, Cuevas, HR, Ontiveros, P, Palet, A, Salazar, SB, Aristizabel, N, Cuadros, A, Tryggvadottir, L, Tulinius, H, Bachelot, A, Le, MG, Peto, J, Franceschi, S, Lubin, F, Modan, B, Ron, E, Wax, Y, Friedman, GD, Hiatt, RA, Levi, F, Bishop, T, Kosmelj, K, Primic-Zakelj, M, Ravnihar, B, Stare, J, Beeson, WL, Fraser, G, Bullbrook, RD, Cuzick, J, Duffy, SW, Fentiman, IS, Hayward, JL, Wang, DY, McMichael, AJ, McPherson, K, Hanson, RL, Leske, MC, Mahoney, MC, Nasca, PC, Varma, AO, Weinstein, AL, Moller, TR, Olsson, H, Ranstam, J, Goldbohm, RA, van den Brandt, PA, Apelo, RA, Baens, J, de la Cruz, JR, Javier, B, Lacaya, LB, Ngelangel, CA, La Vecchia, C, Negri, E, Marubini, E, Ferraroni, M, Gerber, M, Richardson, S, Segala, C, Gatei, D, Kenya, P, Kungu, A, Mati, JG, Brinton, LA, Hoover, R, Schairer, C, Spirtas, R, Lee, HP, Rookus, MA, van Leeuwen, FE, Schoenberg, JA, McCredie, M, Gammon, MD, Clarke, EA, Jones, L, Neil, A, Vessey, M, Yeates, D, Appleby, P, Banks, E, Beral, V, Bull, D, Crossley, B, Goodill, A, Green, J, Hermon, C, Key, T, Langston, N, Lewis, C, Reeves, G, Collins, R, Doll, R, Peto, R, Mabuchi, K, Preston, D, Hannaford, P, Kay, C, Rosero-Bixby, L, Gao, YT, Jin, F, Yuan, JM, Wei, HY, Yun, T, Zhiheng, C, Berry, G, Cooper Booth, J, Jelihovsky, T, MacLennan, R, Shearman, R, Wang, QS, Baines, CJ, Miller, AB, Wall, C, Lund, E, Stalsberg, H, Shu, XO, Zheng, W, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Dabancens, A, Martinez, L, Molina, R, Salas, O, Alexander, FE, Anderson, K, Folsom, AR, Hulka, BS, Bernstein, L, Enger, S, Haile, RW, Paganini-Hill, A, Pike, MC, Ross, RK, Ursin, G, Yu, MC, Longnecker, MP, Newcomb, P, Kalache, A, Farley, TM, Holck, S, Meirik, O, Hamajima, N, Hirose, K, Tajima, K, Rohan, T, Calle, EE, Heath CW, Jr, Coates, RJ, Liff, JM, Talamini, R, Chantarakul, N, Koetsawang, S, Rachawat, D, Morabia, A, Schuman, L, Stewart, W, Szklo, M, Bain, C, Schofield, F, Siskind, V, Band, P, Coldman, AJ, Gallagher, RP, Hislop, TG, Yang, P, Kolonel, LM, Nomura, AM, Hu, J, Johnson, KC, Mao, Y, De Sanjose, S, Lee, N, Marchbanks, P, Ory, HW, Peterson, HB, Wilson, HG, Wingo, PA, Ebeling, K, Kunde, D, Nishan, P, Hopper, JL, Colditz, G, Gajalanski, V, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Ewertz, M, Adami, HO, Bergkvist, L, Magnusson, C, Persson, I, Chang-Claude, J, Paul, C, Skegg, DC, Spears, GF, Boyle, P, Evstifeeva, T, Daling, JR, Hutchinson, WB, Malone, K, Noonan, EA, Stanford, JL, Thomas, DB, Weiss, NS, White, E, Andrieu, N, Bremond, A, Clavel, F, Gairard, B, Lansac, J, Piana, L, Renaud, R, Izquierdo, A, Viladiu, P, Cuevas, HR, Ontiveros, P, Palet, A, Salazar, SB, Aristizabel, N, Cuadros, A, Tryggvadottir, L, Tulinius, H, Bachelot, A, Le, MG, Peto, J, Franceschi, S, Lubin, F, Modan, B, Ron, E, Wax, Y, Friedman, GD, Hiatt, RA, Levi, F, Bishop, T, Kosmelj, K, Primic-Zakelj, M, Ravnihar, B, Stare, J, Beeson, WL, Fraser, G, Bullbrook, RD, Cuzick, J, Duffy, SW, Fentiman, IS, Hayward, JL, Wang, DY, McMichael, AJ, McPherson, K, Hanson, RL, Leske, MC, Mahoney, MC, Nasca, PC, Varma, AO, Weinstein, AL, Moller, TR, Olsson, H, Ranstam, J, Goldbohm, RA, van den Brandt, PA, Apelo, RA, Baens, J, de la Cruz, JR, Javier, B, Lacaya, LB, Ngelangel, CA, La Vecchia, C, Negri, E, Marubini, E, Ferraroni, M, Gerber, M, Richardson, S, Segala, C, Gatei, D, Kenya, P, Kungu, A, Mati, JG, Brinton, LA, Hoover, R, Schairer, C, Spirtas, R, Lee, HP, Rookus, MA, van Leeuwen, FE, Schoenberg, JA, McCredie, M, Gammon, MD, Clarke, EA, Jones, L, Neil, A, Vessey, M, Yeates, D, Appleby, P, Banks, E, Beral, V, Bull, D, Crossley, B, Goodill, A, Green, J, Hermon, C, Key, T, Langston, N, Lewis, C, Reeves, G, Collins, R, Doll, R, Peto, R, Mabuchi, K, Preston, D, Hannaford, P, Kay, C, Rosero-Bixby, L, Gao, YT, Jin, F, Yuan, JM, Wei, HY, Yun, T, Zhiheng, C, Berry, G, Cooper Booth, J, Jelihovsky, T, MacLennan, R, Shearman, R, Wang, QS, Baines, CJ, Miller, AB, Wall, C, Lund, E, Stalsberg, H, Shu, XO, Zheng, W, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Dabancens, A, Martinez, L, Molina, R, Salas, O, Alexander, FE, Anderson, K, Folsom, AR, Hulka, BS, Bernstein, L, Enger, S, Haile, RW, Paganini-Hill, A, Pike, MC, Ross, RK, Ursin, G, Yu, MC, Longnecker, MP, Newcomb, P, Kalache, A, Farley, TM, Holck, S, and Meirik, O

Published
2002

15. Dominant negative ATM mutations in breast cancer families

Author

Chenevix-Trench, G., Spurdle, A. B., Gatei, M., Kelly, H., Marsh, A., Chen, X., Donn, K., Cummings, M., Nyholt, D.R., Jenkins, M. A., Scott, C., Pupo, G. M., Dork, T., Bendix, R., Kirk, J., Tucker, K., McCredie, M. R., Hopper, J. L., Sambrook, J., Mann, G. J., Khanna, K. K., Chenevix-Trench, G., Spurdle, A. B., Gatei, M., Kelly, H., Marsh, A., Chen, X., Donn, K., Cummings, M., Nyholt, D.R., Jenkins, M. A., Scott, C., Pupo, G. M., Dork, T., Bendix, R., Kirk, J., Tucker, K., McCredie, M. R., Hopper, J. L., Sambrook, J., Mann, G. J., and Khanna, K. K.

Abstract

Free to read at publisher's site. BACKGROUND: The ATM gene encoding a putative protein kinase is mutated in ataxia-telangiectasia (A-T), an autosomal recessive disorder with a predisposition for cancer. Studies of A-T families suggest that female heterozygotes have an increased risk of breast cancer compared with noncarriers. However, neither linkage analyses nor mutation studies have provided supporting evidence for a role of ATM in breast cancer predisposition. Nevertheless, two recurrent ATM mutations, T7271G and IVS10-6T-->G, reportedly increase the risk of breast cancer. We examined these two ATM mutations in a population-based, case-control series of breast cancer families and multiple-case breast cancer families. METHODS: Five hundred twenty-five or 262 case patients with breast cancer and 381 or 68 control subjects, respectively, were genotyped for the T7271G and IVS10-6T-->G ATM mutations, as were index patients from 76 non-BRCA1/2 multiple-case breast cancer families. Linkage and penetrance were analyzed. ATM protein expression and kinase activity were analyzed in lymphoblastoid cell lines from mutation carriers. All statistical tests were two-sided. RESULTS: In case and control subjects unselected for family history of breast cancer, one case patient had the T7271G mutation, and none had the IVS10-6T-->G mutation. In three multiple-case families, one of these two mutations segregated with breast cancer. The estimated average penetrance of the mutations was 60% (95% confidence interval [CI] = 32% to 90%) to age 70 years, equivalent to a 15.7-fold (95% CI = 6.4-fold to 38.0-fold) increased relative risk compared with that of the general population. Expression and activity analyses of ATM in heterozygous cell lines indicated that both mutations are dominant negative. CONCLUSION: At least two ATM mutations are associated with a sufficiently high risk of breast cancer to be found in multiple-case breast cancer families. Full mutation analysis of the ATM gene i

Published
2002

18. BRCA1 mutations and other sequence variants in a population-based sample of Australian women with breast cancer

Author

Southey, M. C., Tesoriero, A. A., Andersen, C. R., Jennings, K. M., Brown, S. M., Dite, G. S., Jenkins, M. A., Osborne, R. H., Maskiell, J. A., Porter, L., Giles, G. G., McCredie, M. R. E., Hopper, J. L., Venter, D. J., Southey, M. C., Tesoriero, A. A., Andersen, C. R., Jennings, K. M., Brown, S. M., Dite, G. S., Jenkins, M. A., Osborne, R. H., Maskiell, J. A., Porter, L., Giles, G. G., McCredie, M. R. E., Hopper, J. L., and Venter, D. J.

Published
1999

24. International renal cell cancer study. VII. Role of diet

Author

Wolk, A., Gridley, G., Niwa, S., Lindblad, Per, McCredie, M., Mellemgaard, A., Mandel, J. S., Wahrendorf, J., McLaughlin, J. K., Adami, H. O., Wolk, A., Gridley, G., Niwa, S., Lindblad, Per, McCredie, M., Mellemgaard, A., Mandel, J. S., Wahrendorf, J., McLaughlin, J. K., and Adami, H. O.

Abstract

We investigated the role of diet in the etiology of renal cell cancer (RCC) in a multi-center, population-based case-control study conducted in Australia, Denmark, Sweden and the United States, using a shared protocol. A total of 1,185 incident histopathologically confirmed cases (698 men, 487 women) and 1,526 controls (915 men, 611 women) frequency-matched to cases by sex and age were included in the analyses. The association between RCC and diet was estimated by relative risks (RR) and 95% confidence intervals (CI) adjusted for age, sex, study center, body mass index and smoking. A statistically significant positive association was observed for total energy intake (RR = 1.7, 95% CI = 1.4-2.2 for the highest vs. lowest quartile, p value for trend < 0.00001), while the hypothesis that protein and fat are risk factors independent of energy was not supported. Fried meats were associated with increased RCC risk, while vegetables and fruits were protective, with the strongest effect observed for the highest quartile of consumption of orange/dark green vegetables but not vitamin C or beta carotene. Increased risk was associated with low intake (lowest decile) of vitamin E and magnesium. We observed an apparent protective effect of alcohol confined to women and probably due to chance. Our findings indicate an important role of nutrition in the development of RCC. The apparent positive association of energy intake with risk of RCC needs further investigation in a prospective cohort study to exclude the possible impact of differences in recall between cases and controls.

Published
1996
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25. International renal-cell-cancer study. VI. the role of medical and family history

Author

Schlehofer, B., Pommer, W., Mellemgaard, A., Stewart, J. H., McCredie, M., Niwa, S., Lindblad, Per, Mandel, J. S., McLaughlin, J. K., Wahrendorf, J., Schlehofer, B., Pommer, W., Mellemgaard, A., Stewart, J. H., McCredie, M., Niwa, S., Lindblad, Per, Mandel, J. S., McLaughlin, J. K., and Wahrendorf, J.

Abstract

A number of medical conditions have been linked with renal-cell cancer, although the evidence is not consistent in every case. In a large international case-control study of renal-cell cancer, we examined, among other hypotheses, associations with a personal history of certain medical conditions and a family history of cancer of the kidney or thyroid. Relative risks (RR), adjusted for the effects of age, gender, body-mass index, tobacco smoking and study centre, were significantly increased by a history of kidney stones or thyroid or kidney disease. The RR were not altered by additional adjustment for hypertension, or when diagnoses were restricted to those made at least 5 or 10 years before 1987 (the usual "cut-off" date). The link with kidney injury is particularly likely to be affected by recall bias. Increased RR of borderline significance were found for kidney infection (RR, 1.2) and diabetes (RR, 1.4). Having one first-degree relative with kidney cancer was associated with a significantly increased risk of renal-cell cancer (RR, 1.6; 95% Cl, 1.1-2.4). Seven cases reported 2 first-degree relatives with kidney cancer. No controls had first-degree relatives with kidney cancer. None of our participants reported having von Hippel-Lindau disease. The data suggests that a few conditions of the kidney are strongly associated with renal-cell cancer and that heredity plays a role in a small proportion of cases.

Published
1996
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27. International renal-cell cancer study. V. Reproductive factors, gynecologic operations and exogenous hormones

Author

Lindblad, Per, Mellemgaard, A., Schlehofer, B., Adami, H. O., McCredie, M., McLaughlin, J. K., Mandel, J. S., Lindblad, Per, Mellemgaard, A., Schlehofer, B., Adami, H. O., McCredie, M., McLaughlin, J. K., and Mandel, J. S.

Abstract

The relationships between reproductive factors, exogenous hormones and renal-cell cancer were examined in an international, multicenter, population-based, case-control study undertaken in 1989-1991. Data from 5 centers situated in Australia, Denmark, Germany, Sweden and the United States included for analysis 608 women with renal-cell cancer and 766 female controls. A significant trend in risk (p = 0.002) was associated with number of births, with an 80% excess risk for 6 or more births [RR = 1.8, 95% confidence interval (CI) = 1.1 to 2.9] compared with one birth. A decreasing risk was seen for increasing age at first birth, although this was confounded by body-mass index and number of births. A suggestive reduction of risk was also seen for increasing age at menarche. Age at menopause was unrelated to risk of renal-cell cancer. An increased risk was observed for women having had both a hysterectomy and an oophorectomy. Use of oral contraceptives in non-smoking women reduced the risk of renal-cell cancer (RR = 0.5, 95% CI = 0.4 to 0.8); this reduction increased with longer duration of use. No association was observed for estrogen replacement therapy. Our results indicate that certain hormonal and reproductive variables may be related to risk of renal-cell cancer and deserve further investigation, both epidemiologically and experimentally.

Published
1995
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28. International renal-cell cancer study. III. Role of weight, height, physical activity, and use of amphetamines

Author

Mellemgaard, A., Lindblad, Per, Schlehofer, B., Bergström, R., Mandel, J. S., McCredie, M., McLaughlin, J. K., Niwa, S., Odaka, N., Pommer, W., Mellemgaard, A., Lindblad, Per, Schlehofer, B., Bergström, R., Mandel, J. S., McCredie, M., McLaughlin, J. K., Niwa, S., Odaka, N., and Pommer, W.

Abstract

Although numerous studies have identified obesity or high relative weight as a risk factor for renal-cell cancer in women, the degree to which this effect is present in men remains unclear. A multicenter population-based case-control study concerning incident cases of histologically verified renal-cell cancer (n = 1,732) and age- and sex-matched controls (n = 2,309) was conducted in Australia, Denmark, Germany (2 centers), Sweden and the United States. Relative weight was estimated by the body mass index, and the association between this factor and other factors, such as height, physical activity and use of amphetamines, was measured by the relative risk estimated in logistic regression models. Body mass index was found to be a risk factor among women and, to a lesser extent, among men. A 3-fold increased risk (RR = 3.6, 95% CI = 2.3-5.7) was observed for women with a relative weight in the top 5% compared with those in the lowest quartile. Rate of weight change (estimated as weight change per annum in kilograms) appeared to be an independent risk factor among women but not among men. Physical activity and height were unrelated to risk of renal-cell cancer regardless of level of BMI, while use of amphetamines was associated with an increased risk among men, although no dose or duration effect was seen. Our findings verify the link between high relative weight and risk of renal-cell cancer, particularly among women. The mechanism that underlies this association is, however, still unclear, although the rate of weight change may play a role.

Published
1995
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29. International renal-cell cancer study. VIII. Role of diuretics, other anti-hypertensive medications and hypertension

Author

McLaughlin, J. K., Chow, W. H., Mandel, J. S., Mellemgaard, A., McCredie, M., Lindblad, Per, Schlehofer, B., Pommer, W., Niwa, S., Adami, H. O., McLaughlin, J. K., Chow, W. H., Mandel, J. S., Mellemgaard, A., McCredie, M., Lindblad, Per, Schlehofer, B., Pommer, W., Niwa, S., and Adami, H. O.

Abstract

Risk of renal-cell cancer in relation to use of diuretics, other anti-hypertensive medications and hypertension was assessed in a multi-center, population-based, case-control study conducted in Australia, Denmark, Germany, Sweden and the United States, using a shared protocol and questionnaire. A total of 1,732 histologically confirmed cases and 2,309 controls, frequency-matched to cases by age and sex, were interviewed. The association between renal-cell cancer and the drugs was estimated by relative risks (RRs) and 95% confidence intervals (CIs). Risks were increased among users of diuretics and other anti-hypertensive medications. After adjustment for hypertension, risk for diuretics was reduced to unity, except among long-term (15+ years) users. Risk for use of non-diuretic anti-hypertensive drugs remained significantly elevated and increased further with duration of use. Overall risk was not enhanced when both classes of medications were used. Excess risk was not restricted to any specific type of diuretic or anti-hypertensive drug and no trend was observed with estimated lifetime consumption of any particular type of product. The RR for hypertension after adjustment for diuretics and other anti-hypertensive medications was 1.4 (95% CI = 1.2-1.7), although among non-users of any anti-hypertensive medications, there was little excess risk associated with a history of hypertension. Exclusion of drug use that first occurred within 5 years of cancer diagnosis or interview did not alter the associations. Our findings suggest small effects on renal-cell cancer risk associated with hypertension and use of diuretics and other anti-hypertensive medications. However, because of potential misclassifications of these highly correlated variables, it is difficult to distinguish the effect of treatment from its indication, hypertension.

Published
1995
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30. International renal-cell cancer study. IV. Occupation

Author

Mandel, J. S., McLaughlin, J. K., Schlehofer, B., Mellemgaard, A., Helmert, U., Lindblad, Per, McCredie, M., Adami, H. O., Mandel, J. S., McLaughlin, J. K., Schlehofer, B., Mellemgaard, A., Helmert, U., Lindblad, Per, McCredie, M., and Adami, H. O.

Abstract

The relationship between renal-cell cancer (RCC) and occupation was investigated in an international multicenter population-based case-control study. Study centers in Australia, Denmark, Germany, Sweden and the United States interviewed 1732 incident RCC cases and 2309 controls. Significant associations were found with employment in the blast-furnace or the coke-oven industry [relative risk (RR), 1.7; 95% confidence interval (CI), 1.1-2.7], the iron and steel industry (RR, 1.6; 95% CI, 1.2-2.2) and exposure to asbestos (RR, 1.4; 95% CI, 1.1-1.8), cadmium (RR, 2.0; 95% CI, 1.0-3.9), dry-cleaning solvents (RR, 1.4; 95% CI, 1.1-1.7), gasoline (RR, 1.6; 95% CI, 1.2-2.0) and other petroleum products (RR, 1.6; 95% CI, 1.3-2.1). Asbestos, petroleum products and dry-cleaning solvents appear to merit further investigation, in view of the relationship between risk and duration of employment or exposure and after adjustment for confounding. There was a negative association between RCC and education, but it was not consistent across all centers. Overall, the results of our multicenter case-control study suggest that occupation may be more important in the etiology of RCC than indicated by earlier studies.

Published
1995
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31. International renal-cell cancer study. I. Tobacco use

Author

McLaughlin, J. K., Lindblad, Per, Mellemgaard, A., McCredie, M., Mandel, J. S., Schlehofer, B., Pommer, W., Adami, H. O., McLaughlin, J. K., Lindblad, Per, Mellemgaard, A., McCredie, M., Mandel, J. S., Schlehofer, B., Pommer, W., and Adami, H. O.

Abstract

The relationship between renal-cell cancer (RCC) and tobacco use was investigated in an international, multicenter, population-based case-control study. Coordinated studies were conducted in Australia, Denmark, Germany, Sweden and the United States using a shared protocol and questionnaire. A total of 1,732 cases (1,050 men, 682 women) and 2,309 controls (1,429 men, 880 women) were interviewed for the study. No association was observed between risk and use of cigars, pipes or smokeless tobacco. A statistically significant association was observed for cigarette smoking, with current smokers having a 40% increase in risk [relative risk (RR) = 1.4, 95% confidence interval (CI) 1.2-1.7]. Risk increased with intensity (number of cigarettes) and duration (years smoked). Among current smokers the RR for pack-years rose from 1.1 (95% CI 0.8-1.5) for < 15.9 pack years to 2.0 (95% CI 1.6-2.7) for > 42 pack years (p for trend < 0.001). Long-term quitters (> 15 years) experienced a reduction in risk of about 15-25% relative to current smokers. Those who started smoking late (> 24 years of age) had about two-thirds the risk of those who started young (< or = 12 years of age). Overall, the findings of this pooled analysis confirm that cigarette smoking is a causal factor in the etiology of RCC.

Published
1995
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32. International renal-cell cancer study. II. Analgesics

Author

McCredie, M., Pommer, W., McLaughlin, J. K., Stewart, J. H., Lindblad, Per, Mandel, J. S., Mellemgaard, A., Schlehofer, B., Niwa, S., McCredie, M., Pommer, W., McLaughlin, J. K., Stewart, J. H., Lindblad, Per, Mandel, J. S., Mellemgaard, A., Schlehofer, B., and Niwa, S.

Abstract

There has been concern about the role of analgesics in the development of renal-cell cancer, although a few studies have reported moderately elevated risks with regular or long-term use. In a large international case-control study of renal-cell cancer we examined, among other hypotheses, the effect of phenacetin-containing and of other types of analgesics: paracetamol (acetaminophen), salicylates (mainly aspirin) and pyrazolones (e.g., antipyrine or phenazone). Relative risks, adjusted for the effects of age, sex, body-mass index, tobacco smoking and study centre, were not significantly increased with intake of phenacetin, either when lifetime consumption was categorized at the level of > or = 0.1 kg or when subjects were subdivided further by amount. Nor were paracetamol, salicylates or pyrazolones linked with renal-cell cancer. No consistently increasing risks with consumption level was found. The lack of association was not altered by restricting analgesic use to that which occurred 5 or 10 years before the defined "cut-off" date or when analysis was restricted to exclusive users of a particular type of analgesic. Neither was the risk influenced by the rate of consumption or whether the consumption had occurred at a young age. Our study provides clear evidence that aspirin is unrelated to renal-cell cancer risk, and our findings do not support the hypothesis that analgesics containing phenacetin or paracetamol increase the risk, although the number of "regular" users and the amount of these types of analgesic consumed were too small to confidently rule out a minor carcinogenic effect of phenacetin and paracetamol.

Published
1995
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34. Androgen Receptor Exon 1 CAG Repeat Length and Breast Cancer in Women Before Age Forty Years

Author

Spurdle, A. B., primary, Dite, G. S., additional, Chen, X., additional, Mayne, C. J., additional, Southey, M. C., additional, Batten, L. E., additional, Chy, H., additional, Trute, L., additional, McCredie, M. R. E., additional, Giles, G. G., additional, Armes, J., additional, Venter, D. J., additional, Hopper, J. L., additional, and Chenevix-Trench, G., additional

Published
1999
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37. BRCA1 mutations and other sequence variants in a population-based sample of Australian women with breast cancer

Author

Southey, M C, primary, Tesoriero, A A, additional, Andersen, C R, additional, Jennings, K M, additional, Brown, S M, additional, Dite, G S, additional, Jenkins, M A, additional, Osborne, R H, additional, Maskiell, J A, additional, Porter, L, additional, Giles, G G, additional, McCredie, M R E, additional, Hopper, J L, additional, and Venter, D J, additional

Published
1998
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41. CYP17 promoter polymorphism and breast cancer in Australian women under age forty years.

Author

Spurdle, Amanda B., Hopper, John L., Spurdle, A B, Hopper, J L, Dite, G S, Chen, X, Cui, J, McCredie, M R, Giles, G G, Southey, M C, Venter, D J, Easton, D F, and Chenevix-Trench, G

Subjects
CANCER genetics, CANCER in women, PROMOTERS (Genetics), DNA analysis, AGE distribution, AGE factors in disease, ALLELES, BREAST tumors, COMPARATIVE studies, DNA probes, GENES, GENETIC polymorphisms, RESEARCH methodology, MEDICAL cooperation, GENETIC mutation, ONCOGENES, OXIDOREDUCTASES, POLYMERASE chain reaction, RESEARCH, LOGISTIC regression analysis, EVALUATION research, BRCA genes, RELATIVE medical risk, CASE-control method, GENOTYPES
Abstract

Background: The cytochrome P450c17alpha enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5' promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence breast cancer risk, we conducted a population-based, case-control-family study to assess the relationship between the CYP17 promoter polymorphism and early-onset breast cancer.Methods: Case subjects under 40 years of age at diagnosis of a first primary breast cancer, population-sampled control subjects, and the relatives of both case and control subjects were interviewed to record family history of breast cancer and other risk factors. CYP17 genotype was determined in 369 case subjects, 284 control subjects, and 91 relatives of case subjects. Genotype distributions were compared by logistic regression, and cumulative risk was estimated by a modified segregation analysis. All statistical tests were two-tailed.Results: Compared with the TT genotype (i.e., individuals homozygous for the T allele), the TC genotype was not associated with increased breast cancer risk (P: =.7). Compared with the TT and TC genotypes combined, the CC genotype was associated with a relative risk of 1. 81 (95% confidence interval [CI] = 1.15-2.86; P: =.01) before adjustment for measured risk factors and 1.63 (95% CI = 1.00-2.64; P: =.05) after adjustment. There was an excess of CC genotypes in case subjects who had at least one affected first- or second-degree relative, compared with control subjects unstratified by family history of breast cancer (23% versus 11%; P: =.006), and these case subjects had a threefold to fourfold higher risk than women of other groups defined by genotype and family history of breast cancer. Analysis of breast cancer in first- and second-degree relatives of case subjects with the CC genotype, excluding two known carriers of a deleterious mutation in BRCA1 or BRCA2, gave a relative hazard in women with the CC genotype of 3.48 (95% CI = 1.13-10.74; P: =.04), which is equivalent to a cumulative risk of 16% to age 70 years.Conclusions: The CC genotype may modify the effect of other familial risk factors for early-onset breast cancer. [ABSTRACT FROM AUTHOR]

Published
2000
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42. HRAS1 rare minisatellite alleles and breast cancer in Australian women under age forty years.

Author

Firgaira, Frank A., Seshadri, Ram, Firgaira, F A, Seshadri, R, McEvoy, C R, Dite, G S, Giles, G G, McCredie, M R, Southey, M C, Venter, D J, and Hopper, J L

Subjects
NUCLEOTIDE sequence, ALLELES, BREAST cancer, BREAST tumors, COMPARATIVE studies, GENOMES, RESEARCH methodology, MEDICAL cooperation, PROTEINS, RESEARCH, STATISTICAL sampling, EVALUATION research, CASE-control method, ODDS ratio
Abstract

Background: A recent meta-analysis of 23 studies supported the empirically derived hypothesis that women who lack one of the four common minisatellite alleles at the HRAS1 locus are at increased risk of breast cancer. These studies relied on visual sizing of alleles on electrophoretic gels and may have underreported rare alleles. We determined whether this hypothesis applied to early-onset breast cancer by using a new method to size minisatellite alleles.Methods: We conducted a population-based, case-control-family study of 249 Australian women under 40 years old at diagnosis of a first primary breast cancer and 234 randomly selected women, frequency matched for age. We sized HRAS1 minisatellite alleles with an Applied Biosystems model 373 automated DNA sequencer and GENESCAN(TM) software. All P values are two-sided.Results: We found no association of rare alleles with breast cancer, before or after adjustment for risk factors and irrespective of how their effects were modeled (crude odds ratio = 1.04; 95% confidence interval [CI] = 0.071-1.53; P =.8). The rare allele frequency was 0. 173 (95% CI = 0.149-0.197), three times the pooled estimate of 0.058 (95% CI = 0.050-0.066) from previous studies (P<.001), and was similar for case subjects, 0.177 (95% CI = 0.143-0.221), and control subjects, 0.169 (95% CI = 0.135-0.203) (P =.7).Conclusion: There was no support for an association between rare HRAS1 alleles and the risk of early-onset breast cancer, despite 80% power to detect effects of the magnitude of those associations (1.7-fold) previously suggested.Implications: The question of whether cancer risk is associated with rare minisatellite HRAS1 alleles needs to be revisited with the use of new methods that have a greater ability to distinguish rare alleles from similarly sized common alleles. [ABSTRACT FROM AUTHOR]

Published
1999
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43. Observations on the effect of abolishing analgesic abuse and reducing smoking on cancers of the kidney and bladder in New South Wales, Australia, 1972-1995.

Author

McCredie, M, Stewart, J, Smith, D, Supramaniam, R, and Williams, S

Abstract

Objectives: We have assessed the effect on the rates of cancers of the kidney and bladder of measures undertaken by the government in 1979-1983 to limit smoking and analgesic abuse in New South Wales (NSW). Sale of phenacetin-containing analgesics, previously available without restriction and regularly taken by 11-13% of women and 4-9% of men in NSW, was prohibited from 1979. The prevalence of current smokers among adult Australian men had fallen from 72% in 1945 to 43% in 1980 and to 28% in 1992. In women the corresponding figures were 26%, 31% and 24%.Methods: Incidence and mortality data from the New South Wales Central Cancer Registry for the period 1972 to 1995 were analyzed, by sex and age, for trends over time. Relative survival was calculated for cases diagnosed in the period 1980-94 and followed until the end of 1996.Results: Significant trends evident from these data were: throughout the period of review a rising incidence of, and to a lesser extent mortality from, renal parenchymal cancer for which relative survival has steadily improved; falling mortality from bladder cancer throughout the period of review, but more rapid after 1985; a reversal of the earlier increasing incidence of, and mortality from, cancer of the renal pelvis; and relative survival for bladder and renal pelvic cancers which was worse in women than men. Changes in registration practice in 1985 and 1993 introduced artifacts into the trends in incidence of bladder cancer.Conclusions: Improvements in the trends of incidence and mortality of cancers of the renal pelvis and bladder in the mid-1980s are interpreted, in the light of registration and clinical practice, to indicate a beneficial effect of regulations which virtually abolished analgesic abuse and, less certainly, a contribution from measures restricting smoking, in New South Wales. However, renal parenchymal cancer continues to increase, although there has been some apparent benefit of earlier detection. [ABSTRACT FROM AUTHOR]

Published
1999

44. A case-control study of melanomas of the soles and palms (Australia and Scotland).

Author

Green, Adele, McCredie, Margaret, MacKie, Rona, Giles, Graham, Young, Peta, Morton, Colin, Jackman, Lea, Thursfield, Vicky, Green, A, McCredie, M, MacKie, R, Giles, G, Young, P, Morton, C, Jackman, L, and Thursfield, V

Abstract

Objectives: Because the factors that influence risk of acral melanomas on the soles and palms in White populations are unknown, we investigated these in a multi-center case-control study.Methods: Cases of melanoma of the feet and hands diagnosed from 1987-93 in persons aged over 18 years were ascertained in eastern Australia and western Scotland. There were 275 cases of melanoma on the soles and palms matched to 496 controls (selected from the electoral roll) in Australia, and 36 cases matched to 72 controls (nominated by general practitioners) in Scotland.Results: Acral melanoma was strongly associated with high total body nevus counts (adjusted relative risk [RR] = 6.3, 95% confidence interval [CI] = 2.5-15.6), and with nevi on the soles (RR = 7.5, CI = 3.0-18.6). There were also significant positive associations with a penetrative injury of the feet or hands (RR = 5.0, CI = 3.0-8.6) and with heavy exposure to agricultural chemicals (RR = 3.6, CI = 1.5-8.3). Sun-sensitive complexions, cumulative sun exposure and a past history of nonmelanoma skin cancer were also associated with increased risk of acral melanoma. Current cigarette smoking was inversely related to acral melanoma (RR = 0.6, CI = 0.4-0.9).Conclusions: Melanomas of the soles and palms resemble other cutaneous melanomas in their association with sun exposure, but are distinguished from them by their strong positive associations with nevi on the soles, previous penetrative injury, and exposure to agricultural chemicals, and by their inverse association with smoking. [ABSTRACT FROM AUTHOR]

Published
1999
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45. Estrogen receptor polymorphism at codon 325 and risk of breast cancer in women before age forty.

Author

Southey, M C, Batten, L E, McCredie, M R, Giles, G G, Dite, G, Hopper, J L, and Venter, D J

Subjects
ALLELES, BREAST tumors, COMPARATIVE studies, DNA probes, GENES, GENETIC polymorphisms, RESEARCH methodology, MEDICAL cooperation, PROTEINS, RESEARCH, EVALUATION research, CASE-control method, ODDS ratio
Abstract

Background: The estrogen receptor (ER) protein is believed to play a role in the development and progression of breast cancer. In a previously published U.S. clinic-based study, a polymorphism in the ER gene (codon 325, CCC --> CCG) was found to be more common in 34 case subjects with a family history of breast cancer than in 154 case subjects without such a history (mean allele frequencies +/- standard error = 0.28+/-0.05 versus 0.11+/-0.02; P<.001). To determine whether this polymorphism is a risk factor for early-onset breast cancer, we conducted a population-based, case-control-family study in Australia.Methods: Case subjects under the age of 40 years with a first primary breast cancer and control subjects, frequency-matched to the case subjects on the basis of age, and their relatives were interviewed to assess the family history of breast cancer. Polymorphism status of the ER gene was determined for 388 case subjects and 294 control subjects. All statistical tests were two-tailed.Results: There was no association between ER gene polymorphism status and breast cancer, before or after adjustment for risk factors. There was no difference in allele frequencies between case subjects and control subjects (0.232+/-0.015 versus 0.209+/-0.017; P = .4) or between women with and without a family history of breast cancer (P = .3), irrespective of case-control status. The findings were not altered when different definitions of family history of breast cancer were used and when allele frequencies were adjusted for residence and country of birth.Conclusion: We found no evidence that the ER codon 325 polymorphism is associated with breast cancer before the age of 40 years or with a family history of breast cancer, despite ample power to detect effects half the magnitude of those previously reported. [ABSTRACT FROM AUTHOR]

Published
1998
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46. Breast cancer in Australian women under the age of 40.

Author

McCredie, Margaret, Dite, Gillian, Giles, Graham, Hopper, John, McCredie, M R, Dite, G S, Giles, G G, and Hopper, J L

Abstract

Objectives: A case-control-family study of breast cancer in women under the age of 40 was carried out in Melbourne and Sydney, Australia, from 1992 to 1995 to determine the risk factors for these women. Subjects included 467 incident cases identified by state cancer registries and 408 population-based controls.Methods: All participants completed a structured risk-factor questionnaire and family pedigree during an in-person interview. Where possible, cancers in first- and second-degree relatives were verified.Results: Multiple logistic regression analysis showed that the strongest risk factor for breast cancer was a family history of the disease -- having at least one affected first-degree relative trebled the risk (relative risk [RR] = 3.3, 95 percent confidence interval [CI] = 1.9-5.8). Risk increased with height by three percent (standard error [SE] of one percent) per cm, and after adjusting for height, there was evidence for a decreased risk in women weighing 73 kg or more. There was an increased risk of breast cancer after the first full-term birth (RR = 1.8, CI = 1.0-3.5) but this risk fell by 30 percent (SE = 11 percent) with each subsequent livebirth.Conclusions: The effects of other reproductive factors and oral contraceptive use, although not nominally significant, were in accord with published findings from similar studies in young women. This study of Australian women has indicated that some risk factors for breast cancer in women under age 40 differ from those reported for older women either in direction (e.g., weight) or relative importance (e.g., family history). [ABSTRACT FROM AUTHOR]

Published
1998
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47. BRCA1 mutations and other sequence variants in a population-based sample of Australian women with breast cancer.

Author

Southey, M C, Tesoriero, A A, Andersen, C R, Jennings, K M, Brown, S M, Dite, G S, Jenkins, M A, Osborne, R H, Maskiell, J A, Porter, L, Giles, G G, McCredie, M R E, Hopper, J L, and Venter, D J

Subjects
BREAST cancer, GENETIC mutation
Abstract

The frequency, in women with breast cancer, of mutations and other variants in the susceptibility gene, BRCA1, was investigated using a population-based case-control-family study. Cases were women living in Melbourne or Sydney, Australia, with histologically confirmed, first primary, invasive breast cancer, diagnosed before the age of 40 years, recorded on the state Cancer Registries. Controls were women without breast cancer, frequency-matched for age, randomly selected from electoral rolls. Full manual sequencing of the coding region ofBRCA1 was conducted in a randomly stratified sample of 91 cases; 47 with, and 44 without, a family history of breast cancer in a first- or second-degree relative. All detected variants were tested in a random sample of 67 controls. Three cases with a (protein-truncating) mutation were detected. Only one case had a family history; her mother had breast cancer, but did not carry the mutation. The proportion of Australian women with breast cancer before age 40 who carry a germline mutation inBRCA1 was estimated to be 3.8% (95% Cl 0.3-12.6%). Seven rare variants were also detected, but for none was there evidence of a strong effect on breast cancer susceptibility. Therefore, on a population basis, rare variants are likely to contribute little to breast cancer incidence. [ABSTRACT FROM AUTHOR]

Published
1999
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49. Percutaneous transluminal balloon dilatation of the mitral valve in pregnancy.

Author

Smith, R, Brender, D, and McCredie, M

Abstract

Pregnancy can cause life threatening complications in women with mitral stenosis, and there is a substantial risk of fetal death if valvotomy under cardiopulmonary bypass is required. A patient is described in whom pulmonary oedema developed after delivery of her first child by caesarean section 13 months previously. Subsequent cardiac catheterisation showed severe mitral stenosis (valve area 0.96 cm2, valve gradient 12 mm Hg, pulmonary artery pressure 30/16 mm Hg). Before valvotomy could be performed the patient again became pregnant and presented in pulmonary oedema at twenty two weeks' gestation. Medical treatment was unsuccessful and she underwent percutaneous transluminal balloon dilatation of the mitral valve. This increased the valve area to 1.78 cm2 and reduced the transmitral gradient to 6 mm Hg. The procedure was uncomplicated, and she remained symptom free on no medication. She delivered vaginally at 37 weeks' gestation. Percutaneous transluminal balloon dilatation of the mitral valve is a safe and effective alternative to mitral valvotomy in pregnancy. [ABSTRACT FROM PUBLISHER]

Published
1989
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