Louise A Brinton1, Tim J Key2, Laurence N Kolonel2, Karin B Michels2, Howard D Sesso2, Giske Ursin2, Stephen K Van Den Eeden2, Shannon N Wood2, Roni T Falk2, Dominick Parisi2, Chantal Guillemette2, Patrick Caron2, Véronique Turcotte2, Laurel A Habel2, Claudine J Isaacs2, Elio Riboli2, Elisabete Weiderpass2, Michael B Cook2. 1. Louise A. Brinton, Shannon N. Wood, Roni T. Falk, and Michael B. Cook, National Cancer Institute, Bethesda; Dominick Parisi, Information Management Services, Rockville, MD; Tim J. Key, University of Oxford, Oxford; Elio Riboli, Imperial College School of Public Health, London, United Kingdom; Laurence N. Kolonel, University of Hawaii, Honolulu, HI; Karin B. Michels, Harvard Medical School and Harvard School of Public Health; Karin B. Michels and Howard D. Sesso, Brigham and Women's Hospital, Boston, MA; Giske Ursin, University of Oslo; Giske Ursin and Elisabete Weiderpass, Cancer Registry of Norway, Oslo; University of Tromsø-Arctic University of Norway, Tromsø, Norway; Karolinska Institutet, Stockholm, Sweden; and Samfundet Folkhalsan, Helsinki, Finland; Giske Ursin, University of Southern California, Los Angeles; Stephen K. Van Den Eeden and Laurel A. Habel, Kaiser Permanente Northern California, Oakland, CA; Chantal Guillemette, Patrick Caron, and Véronique Turcotte, Centre Hospitalier Universitaire de Québec and Laval University, Québec City, Québec, Canada; and Claudine J. Isaacs, Georgetown University, Washington, DC. brinton@nih.gov. 2. Louise A. Brinton, Shannon N. Wood, Roni T. Falk, and Michael B. Cook, National Cancer Institute, Bethesda; Dominick Parisi, Information Management Services, Rockville, MD; Tim J. Key, University of Oxford, Oxford; Elio Riboli, Imperial College School of Public Health, London, United Kingdom; Laurence N. Kolonel, University of Hawaii, Honolulu, HI; Karin B. Michels, Harvard Medical School and Harvard School of Public Health; Karin B. Michels and Howard D. Sesso, Brigham and Women's Hospital, Boston, MA; Giske Ursin, University of Oslo; Giske Ursin and Elisabete Weiderpass, Cancer Registry of Norway, Oslo; University of Tromsø-Arctic University of Norway, Tromsø, Norway; Karolinska Institutet, Stockholm, Sweden; and Samfundet Folkhalsan, Helsinki, Finland; Giske Ursin, University of Southern California, Los Angeles; Stephen K. Van Den Eeden and Laurel A. Habel, Kaiser Permanente Northern California, Oakland, CA; Chantal Guillemette, Patrick Caron, and Véronique Turcotte, Centre Hospitalier Universitaire de Québec and Laval University, Québec City, Québec, Canada; and Claudine J. Isaacs, Georgetown University, Washington, DC.
Abstract
PURPOSE: Although previous studies have implicated a variety of hormone-related risk factors in the etiology of male breast cancers, no previous studies have examined the effects of endogenous hormones. PATIENTS AND METHODS: Within the Male Breast Cancer Pooling Project, an international consortium comprising 21 case-control and cohort investigations, a subset of seven prospective cohort studies were able to contribute prediagnostic serum or plasma samples for hormone quantitation. Using a nested case-control design, multivariable unconditional logistic regression analyses estimated odds ratios and 95% CIs for associations between male breast cancer risk and 11 individual estrogens and androgens, as well as selected ratios of these analytes. RESULTS: Data from 101 cases and 217 matched controls were analyzed. After adjustment for age and date of blood draw, race, and body mass index, androgens were found to be largely unrelated to risk, but circulating estradiol levels showed a significant association. Men in the highest quartile had an odds ratio of 2.47 (95% CI, 1.10 to 5.58) compared with those in the lowest quartile (trend P = .06). Assessment of estradiol as a ratio to various individual androgens or sum of androgens showed no further enhancement of risk. These relations were not significantly modified by either age or body mass index, although estradiol was slightly more strongly related to breast cancers occurring among younger (age < 67 years) than older men. CONCLUSION: Our results support the notion of an important role for estradiol in the etiology of male breast cancers, similar to female breast cancers.
PURPOSE: Although previous studies have implicated a variety of hormone-related risk factors in the etiology of male breast cancers, no previous studies have examined the effects of endogenous hormones. PATIENTS AND METHODS: Within the Male Breast Cancer Pooling Project, an international consortium comprising 21 case-control and cohort investigations, a subset of seven prospective cohort studies were able to contribute prediagnostic serum or plasma samples for hormone quantitation. Using a nested case-control design, multivariable unconditional logistic regression analyses estimated odds ratios and 95% CIs for associations between male breast cancer risk and 11 individual estrogens and androgens, as well as selected ratios of these analytes. RESULTS: Data from 101 cases and 217 matched controls were analyzed. After adjustment for age and date of blood draw, race, and body mass index, androgens were found to be largely unrelated to risk, but circulating estradiol levels showed a significant association. Men in the highest quartile had an odds ratio of 2.47 (95% CI, 1.10 to 5.58) compared with those in the lowest quartile (trend P = .06). Assessment of estradiol as a ratio to various individual androgens or sum of androgens showed no further enhancement of risk. These relations were not significantly modified by either age or body mass index, although estradiol was slightly more strongly related to breast cancers occurring among younger (age < 67 years) than older men. CONCLUSION: Our results support the notion of an important role for estradiol in the etiology of male breast cancers, similar to female breast cancers.
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