Browsing by Author "D. Bull"

Filter results by typing the first few letters
Now showing 1 - 4 of 4
  • No Thumbnail Available
    PublicationMetadata only
    Menarche, menopause, and breast cancer risk: Individual participant meta-analysis, including 118 964 women with breast cancer from 117 epidemiological studies
    (2012-01-01) N. Hamajima; K. Hirose; K. Tajima; T. Rohan; C. M. Friedenreich; E. E. Calle; S. M. Gapstur; A. V. Patel; R. J. Coates; J. M. Liff; R. Talamini; N. Chantarakul; S. Koetsawang; D. Rachawat; Y. Marcou; E. Kakouri; S. W. Duffy; A. Morabia; L. Schuman; W. Stewart; M. Szklo; P. F. Coogan; J. R. Palmer; L. Rosenberg; P. Band; A. J. Coldman; R. P. Gallagher; T. G. Hislop; P. Yang; S. R. Cummings; K. Canfell; F. Sitas; P. Chao; J. Lissowska; P. L. Horn-Ross; E. M. John; L. M. Kolonel; A. M.Y. Nomura; R. Ghiasvand; J. Hu; K. C. Johnson; Y. Mao; V. Beral; D. Bull; K. Callaghan; B. Crossley; A. Goodill; J. Green; C. Hermon; T. Key; I. Lindgard; B. Liu; K. Pirie; G. Reeves; R. Collins; R. Doll; R. Peto; T. Bishop; I. S. Fentiman; S. De Sanjosé; C. A. Gonzalez; N. Lee; P. Marchbanks; H. W. Ory; H. B. Peterson; P. Wingo; K. Ebeling; D. Kunde; P. Nishan; J. L. Hopper; H. Eliassen; S. Hankinson; V. Gajalakshmi; N. Martin; T. Pardthaisong; S. Silpisornkosol; C. Theetranont; B. Boosiri; S. Chutivongse; P. Jimakorn; P. Virutamasen; C. Wongsrichanalai; A. Neugut; R. Santella; C. J. Baines; N. Kreiger; A. B. Miller; C. Wall; A. Tjonneland; T. Jorgensen; C. Stahlberg; A. Tønnes Pedersen; D. Flesch-Janys; N. Hakansson; J. Cauley; I. Heuch; H. O. Adami; I. Persson; E. Weiderpass; C. Magnusson; Aichi Cancer Center Hospital and Research Institute; Albert Einstein College of Medicine of Yeshiva University; Alberta Health Services; American Cancer Society; Emory University; IRCCS Centro Di Riferimento Oncologico Aviano; Mahidol University; Bank of Cyprus Group Oncology Centre; Barts and The London Queen Mary's School of Medicine and Dentistry; Johns Hopkins University; Boston University; British Columbia Cancer Agency; California Pacific Medical Center; Cancer Council New South Wales; Institute of Oncology, Warsaw; Cancer Prevention Institute of California; University of Hawaii System; University of Tehran; Canadian Cancer Registries Epidemiology Research Group; Cancer Research UK; Clinical Trial Service Unit; Catalan Oncology Institute; Centers for Disease Control and Prevention; Max Delbruck Center for Molecular Medicine; University of Melbourne; Brigham and Women's Hospital; Cancer Institute India; Chiang Mai University; Chulalongkorn University; Columbia University in the City of New York; Dalla Lana School of Public Health; Institute of Cancer Epidemiology - Denmark; Danish Nurse Cohort Study; Universitatsklinikum Hamburg-Eppendorf und Medizinische Fakultat; Karolinska Institutet; University of Pittsburgh; Universitetet i Bergen; German Cancer Research Center; University of Otago; National Cancer Center Tokyo; Fred Hutchinson Cancer Research Center; Epidemiology Unit and Girona Cancer Registry (UERCG); UCL; Hospital General de Mexico; Hospital Universitario; Icelandic Cancer Society; Imperial College London; Institut de Cancerologie Gustave Roussy; Inserm; Instituto Nacional de Salud Publica; International Agency for Research on Cancer; International Prevention Research Institute; Chaim Sheba Medical Center Israel; Kaiser Permanente; Institut Universitaire de Medecine Sociale et Preventive Lausanne; Onkoloski institut Ljubljana; Loma Linda University Adventist Health Sciences Center; London School of Hygiene & Tropical Medicine; Long Island Breast Cancer Study; Skånes universitetssjukhus; Maastricht University; ISPO; Icahn School of Medicine at Mount Sinai; University of the Philippines Manila; Universita degli Studi di Milano; Fondazione IRCCS Istituto Nazionale dei Tumori, Milan; Istituto di Statistica Medica e Biometria; Memorial Sloan-Kettering Cancer Center; Nairobi Centre for Research in Reproduction; National Cancer Institute; Australian National University; National Institute of Child Health and Human Development; National University of Singapore; The Netherlands Cancer Institute; New Jersey State Department of Health; Norwegian Institute of Public Health; Department of Public Health; Radiation Effects Research Foundation Hiroshima; Royal College of General Practitioners Oral Contraception Study; Roswell Park Cancer Institute; Universidad de Costa Rica; Medical Center of Fudan University; Shanghai Institute of Planned Parenthood Research; Cyprus Institute of Neurology and Genetics; Wuhan University; Tianjin Cancer Institute and Hospital; Tohoku University School of Medicine; Universitetet i Tromso; Vanderbilt University; University Medical Center Utrecht; University of Athens Medical School; University of California, San Francisco; Universidad de Chile; University of Edinburgh; University of Minnesota School of Public Health; The University of North Carolina at Chapel Hill; University of Nottingham; Universita degli Studi di Padova; University of Queensland; University of Pennsylvania, School of Medicine; University of Southern California; Syddansk Universitet; University of Toronto; Women's Health Initiative; Organisation Mondiale de la Sante; Yamagata University Faculty of Medicine
    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 receptorpositive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours.
  • No Thumbnail Available
    PublicationMetadata only
    Ovarian cancer and body size: Individual participant meta-analysis including 25,157 women with ovarian cancer from 47 epidemiological studies
    (2012-04-01) V. Beral; C. Hermon; R. Peto; G. Reeves; L. Brinton; P. Marchbanks; E. Negri; R. B. Ness; P. H.M. Peeters; M. Vessey; E. E. Calle; S. M. Gapstur; A. V. Patel; L. Dal Maso; R. Talamini; A. Chetrit; G. Hirsh-Yechezkel; F. Lubin; S. Sadetzki; N. Allen; D. Bull; K. Callaghan; B. Crossley; K. Gaitskell; A. Goodill; J. Green; T. Key; K. Moser; R. Collins; R. Doll; C. A. Gonzalez; N. Lee; H. W. Ory; H. B. Peterson; P. A. Wingo; N. Martin; T. Pardthaisong; S. Silpisornkosol; C. Theetranont; B. Boosiri; S. Chutivongse; P. Jimakorn; P. Virutamasen; C. Wongsrichanalai; A. Tjonneland; L. Titus-Ernstoff; T. Byers; T. Rohan; B. J. Mosgaard; D. Yeates; J. L. Freudenheim; J. Chang-Claude; R. Kaaks; K. E. Anderson; A. Folsom; M. A. Rossing; D. B. Thomas; N. S. Weiss; E. Riboli; F. Clavel-Chapelon; D. Cramer; K. Robien; S. S. Tworoger; D. Cramer; S. E. Hankinson; S. S. Tworoger; S. Franceschi; C. La Vecchia; C. Magnusson; T. Riman; E. Weiderpass; A. Wolk; L. J. Schouten; P. A. Van den Brandt; N. Chantarakul; S. Koetsawang; D. Rachawat; D. Palli; A. Black; A. Berrington de Gonzalez; D. M. Freedman; P. Hartge; A. W. Hsing; J. V. Lacey; R. N. Hoover; C. Schairer; S. Graff-Iversen; R. Selmer; C. J. Bain; A. C. Green; D. M. Purdie; V. Siskind; P. M. Webb; American Cancer Society; IRCCS Centro Di Riferimento Oncologico Aviano; The Gertner Institute; Cancer Epidemiology Unit; Clinical Trial Service Unit; Institute Catala Oncologia; Centers for Disease Control and Prevention; Chiang Mai University; Chulalongkorn University; Institute of Cancer Epidemiology - Denmark; Geisel School of Medicine at Dartmouth; Colorado School of Public Health; Albert Einstein College of Medicine of Yeshiva University; Amtssygehuset i Herlev; Department of Public Health; University at Buffalo, State University of New York; German Cancer Research Center; University of Minnesota School of Public Health; University of Washington, Seattle; Imperial College London; Centre de recherche en epidemiologie et sante des populations; Harvard Medical School; Brigham and Women's Hospital; Channing Laboratory; International Agency for Research on Cancer; Universita degli Studi di Milano; Karolinska Institutet; Maastricht University; Mahidol University; Centro Per Lo Studio E La Prevenzione Oncologica; National Cancer Institute; Norwegian Institute of Public Health; Queensland Institute of Medical Research; Roswell Park Cancer Institute; Royal College of General Practitioners' Oral Contraception Study; Curtin University; University of Texas System; University of Massachusetts System; Boston University; Stanford University; University of Athens Medical School; Universidad de Chile; University of Hawaii System; Skånes universitetssjukhus; University of Pennsylvania; University Medical Center Utrecht; University of Southern California; University of Toronto; Universitetet i Tromso; George Washington University; Vanderbilt University; Organisation Mondiale de la Sante; Yale University
    Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p < 0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p < 0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m 2 increase in body mass index was 1.10 (95% CI, 1.07-1.13; p < 0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ovarian cancer incidence per decade. © 2012 Collaborative Group on Epidemiological Studies of Ovarian Cancer.
  • No Thumbnail Available
    PublicationMetadata only
    Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23 257 women with ovarian cancer and 87 303 controls
    (2008-01-26) V. Beral; R. Doll; C. Hermon; R. Peto; G. Reeves; L. Brinton; A. C. Green; P. Marchbanks; E. Negri; R. Ness; P. Peeters; M. Vessey; E. E. Calle; C. Rodriguez; L. Dal Maso; R. Talamini; D. Cramer; S. E. Hankinson; S. S. Tworoger; A. Chetrit; G. Hirsh-Yechezkel; F. Lubin; S. Sadetzki; P. Appleby; E. Banks; A. Berrington de Gonzalez; D. Bull; B. Crossley; A. Goodill; I. Green; J. Green; T. Key; R. Collins; C. A. Gonzalez; N. Lee; H. W. Ory; H. B. Peterson; P. A. Wingo; N. Martin; T. Pardthaisong; S. Silpisornkosol; C. Theetranont; B. Boosiri; S. Chutivongse; P. Jimakorn; P. Virutamasen; C. Wongsrichanalai; L. Titus-Ernstoff; B. J. Mosgaard; D. Yeates; J. Chang-Claude; M. A. Rossing; D. Thomas; N. Weiss; S. Franceschi; C. La Vecchia; H. O. Adami; C. Magnusson; T. Riman; E. Weiderpass; A. Wolk; L. A. Brinton; D. M. Freedman; P. Hartge; J. M. Lacey; R. Hoover; L. J. Schouten; P. A. van den Brandt; N. Chantarakul; S. Koetsawang; D. Rachawat; S. Graff-Iversen; R. Selmer; C. J. Bain; D. M. Purdie; V. Siskind; P. M. Webb; S. E. McCann; P. Hannaford; C. Kay; C. W. Binns; A. H. Lee; M. Zhang; P. Nasca; P. F. Coogan; L. Rosenberg; J. Kelsey; R. Paffenbarger; A. Whittemore; K. Katsouyanni; A. Trichopoulou; D. Trichopoulos; A. Tzonou; A. Dabancens; L. Martinez; R. Molina; O. Salas; M. T. Goodman; G. Laurie; American Cancer Society; IRCCS Centro Di Riferimento Oncologico Aviano; Brigham and Women's Hospital; Channing Laboratory; The Gertner Institute; Cancer Epidemiology Unit; Clinical Trial Service Unit; Institute Catala Oncologia; Centers for Disease Control and Prevention; Chiang Mai University; Chulalongkorn University; Geisel School of Medicine at Dartmouth; Amtssygehuset i Herlev; Department of Public Health; German Cancer Research Center; University of Washington, Seattle; International Agency for Research on Cancer; Universita degli Studi di Milano; Karolinska Institutet; National Cancer Institute; Maastricht University; Mahidol University; Norwegian Institute of Public Health; University of Queensland; Roswell Park Cancer Institute; Royal College of General Practitioners Oral Contraception Study; Curtin University; University of Massachusetts System; Boston University; Stanford University; University of Athens Medical School; Universidad de Chile; University of Hawaii System; Skånes universitetssjukhus; University of Pittsburgh; University of Pennsylvania; University Medical Center Utrecht; University of Southern California; Universitetet i Tromso; Vanderbilt University; Organisation Mondiale de la Sante; Yale University
    Background: Oral contraceptives were introduced almost 50 years ago, and over 100 million women currently use them. Oral contraceptives can reduce the risk of ovarian cancer, but the eventual public-health effects of this reduction will depend on how long the protection lasts after use ceases. We aimed to assess these effects. Methods: Individual data for 23 257 women with ovarian cancer (cases) and 87 303 without ovarian cancer (controls) from 45 epidemiological studies in 21 countries were checked and analysed centrally. The relative risk of ovarian cancer in relation to oral contraceptive use was estimated, stratifying by study, age, parity, and hysterectomy. Findings: Overall 7308 (31%) cases and 32 717 (37%) controls had ever used oral contraceptives, for average durations among users of 4·4 and 5·0 years, respectively. The median year of cancer diagnosis was 1993, when cases were aged an average of 56 years. The longer that women had used oral contraceptives, the greater the reduction in ovarian cancer risk (p<0·0001). This reduction in risk persisted for more than 30 years after oral contraceptive use had ceased but became somewhat attenuated over time-the proportional risk reductions per 5 years of use were 29% (95% CI 23-34%) for use that had ceased less than 10 years previously, 19% (14-24%) for use that had ceased 10-19 years previously, and 15% (9-21%) for use that had ceased 20-29 years previously. Use during the 1960s, 1970s, and 1980s was associated with similar proportional risk reductions, although typical oestrogen doses in the 1960s were more than double those in the 1980s. The incidence of mucinous tumours (12% of the total) seemed little affected by oral contraceptives, but otherwise the proportional risk reduction did not vary much between different histological types. In high-income countries, 10 years use of oral contraceptives was estimated to reduce ovarian cancer incidence before age 75 from 1·2 to 0·8 per 100 users and mortality from 0·7 to 0·5 per 100; for every 5000 woman-years of use, about two ovarian cancers and one death from the disease before age 75 are prevented. Interpretation: Use of oral contraceptives confers long-term protection against ovarian cancer. These findings suggest that oral contraceptives have already prevented some 200 000 ovarian cancers and 100 000 deaths from the disease, and that over the next few decades the number of cancers prevented will rise to at least 30 000 per year. © 2008 Elsevier Ltd. All rights reserved.
  • No Thumbnail Available
    PublicationMetadata only
    Ovarian cancer and smoking: Individual participant meta-analysis including 28 114 women with ovarian cancer from 51 epidemiological studies
    (2012-01-01) E. E. Calle; S. M. Gapstur; A. V. Patel; L. Dal Maso; R. Talamini; A. Chetrit; G. Hirsh-Yechezkel; F. Lubin; S. Sadetzki; E. Banks; V. Beral; D. Bull; K. Callaghan; B. Crossley; K. Gaitskell; A. Goodill; J. Green; C. Hermon; T. Key; K. Moser; G. Reeves; F. Sitas; R. Collins; R. Doll; R. Peto; C. A. Gonzalez; N. Lee; P. Marchbanks; H. W. Ory; H. B. Peterson; P. A. Wingo; N. Martin; T. Pardthaisong; S. Silpisornkosol; C. Theetranont; B. Boosiri; S. Chutivongse; P. Jimakorn; P. Virutamasen; C. Wongsrichanalai; A. Tjonneland; L. Titus-Ernstoff; T. Byers; T. Rohan; B. J. Mosgaard; M. Vessey; D. Yeates; J. L. Freudenheim; J. Chang-Claude; R. Kaaks; K. E. Anderson; A. Folsom; K. Robien; J. Hampton; P. A. Newcomb; M. A. Rossing; D. B. Thomas; N. S. Weiss; E. Riboli; F. Clavel-Chapelon; D. Cramer; S. E. Hankinson; S. S. Tworoger; S. Franceschi; C. La Vecchia; E. Negri; H. O. Adami; C. Magnusson; T. Riman; E. Weiderpass; A. Wolk; L. J. Schouten; P. A. van den Brandt; N. Chantarakul; S. Koetsawang; D. Rachawat; D. Palli; A. Black; L. A. Brinton; D. M. Freedman; P. Hartge; A. W. Hsing; Jr V. Lacey; R. N. Hoover; C. Schairer; M. Urban; S. Graff-Iversen; R. Selmer; C. J. Bain; A. C. Green; D. M. Purdie; V. Siskind; P. M. Webb; K. Moysich; S. E. McCann; P. Hannaford; C. Kay; C. W. Binns; A. H. Lee; M. Zhang; American Cancer Society; IRCCS Centro Di Riferimento Oncologico Aviano; The Gertner Institute; The National Israeli Study on Ovarian Cancer (NISOC) group; Cancer Council New South Wales; Cancer Research UK; Institute Catala Oncologia; Centers for Disease Control and Prevention; Chiang Mai University; Chulalongkorn University; Institute of Cancer Epidemiology - Denmark; Geisel School of Medicine at Dartmouth; Colorado School of Public Health; Albert Einstein College of Medicine of Yeshiva University; Amtssygehuset i Herlev; Department of Public Health; University at Buffalo, State University of New York; German Cancer Research Center; University of Minnesota School of Public Health; University of Washington, Seattle; Imperial College London; Centre de recherche en epidemiologie et sante des populations; Harvard Medical School; International Agency for Research on Cancer; Universita degli Studi di Milano; Karolinska Institutet; Maastricht University; Mahidol University; Centro Per Lo Studio E La Prevenzione Oncologica; National Cancer Institute; National Health Laboratory Services; Norwegian Institute of Public Health; Queensland Institute of Medical Research; Roswell Park Cancer Institute; Royal College of General Practitioners' Oral Contraception Study; Curtin University; University of Texas School of Public Health; University of Massachusetts Boston; Boston University - Slone Epidemiology Unit; Stanford University; University of Athens Medical School; Universidad de Chile; University of Hawaii at Manoa; Skånes universitetssjukhus; University of Pennsylvania; University of Pittsburgh; University Medical Center Utrecht; University of Southern California; University of Toronto; Universitetet i Tromso; George Washington University; Vanderbilt University; Organisation Mondiale de la Sante; Yale University
    Background Smoking has been linked to mucinous ovarian cancer, but its eff ects on other ovarian cancer subtypes and on overall ovarian cancer risk are unclear, and the fi ndings from most studies with relevant data are unpublished. To assess these associations, we review the published and unpublished evidence. Methods Eligible epidemiological studies were identifi ed by electronic searches, review articles, and discussions with colleagues. Individual participant data for 28 114 women with and 94 942 without ovarian cancer from 51 epidemiological studies were analysed centrally, yielding adjusted relative risks (RRs) of ovarian cancer in smokers compared with never smokers. Findings After exclusion of studies with hospital controls, in which smoking could have aff ected recruitment, overall ovarian cancer incidence was only slightly increased in current smokers compared with women who had never smoked (RR 1.06, 95% CI 1.01-1.11, p=0.01). Of 17 641 epithelial cancers with specifi ed histology, 2314 (13%) were mucinous, 2360 (13%) endo metrioid, 969 (5%) clear-cell, and 9086 (52%) serous. Smoking-related risks varied substantially across these subtypes (p heterogeneity < 0.0001). For mucinous cancers, incidence was increased in current versus never smokers (1.79, 95% CI 1.60-2.00, p < 0.0001), but the increase was mainly in borderline malignant rather than in fully malignant tumours (2.25, 95% CI 1.91-2.65 vs 1.49, 1.28-1.73; p heterogeneity =0.01; almost half the mucinous tumours were only borderline malignant). Both endometrioid (0.81, 95% CI 0.72-0.92, p=0.001) and clear-cell ovarian cancer risks (0.80, 95% CI 0.65-0.97, p=0.03) were reduced in current smokers, and there was no signifi cant association for serous ovarian cancers (0.99, 95% CI 0.93-1.06, p=0.8). These associations did not vary signifi cantly by 13 sociodemographic and personal characteristics of women including their body-mass index, parity, and use of alcohol, oral contraceptives, and menopausal hormone therapy. Interpretation The excess of mucinous ovarian cancers in smokers, which is mainly of tumours of borderline malignancy, is roughly counterbalanced by the defi cit of endometrioid and clear-cell ovarian cancers. The substantial variation in smoking-related risks by tumour subtype is important for understanding ovarian carcinogenesis.