INTRODUCTION: Obesity is a well-established risk factor for postmenopausal breast cancer, but mechanisms underlying the association are unclear. Adipocyte-derived, cytokine-like adipokines have been suggested as contributory factors. To evaluate their association with breast cancer risk factors and breast cancer risk, we conducted a nested case-control study of 234 postmenopausal breast cancer cases and 234 controls in a cohort of U.S. women with prospectively-collected serum samples obtained in the mid 1970s and followed for up to 25 years. METHODS: Adiponectin, absolute plasminogen activator inhibitor-1 (aPAI-1), and resistin were measured by a multiplex immunoassay. Sex hormones were available for 67 cases and 67 controls. RESULTS: Among controls, we found that lower levels of adiponectin and higher levels of aPAI-1 were correlated with increasing levels of estradiol (Spearman r=-0.26, p-value=0.033; r=0.42, p=0.0003), decreasing levels of sex hormone binding globulin (r=0.38, p=0.0013; r=-0.32, p=0.0076), and increasing body mass index (BMI) (r=-0.31, p=<0.0001; r=0.39, p=<0.0001). Hormones were not associated with resistin. Among the relatively small percentage of women using postmenopausal hormones at the time of blood collection (13.7%), aPAI-1 levels were higher than in non-users (p=0.0054). Breast cancer risk was not associated with circulating levels of adiponectin (age-adjusted p for linear trend=0.43), aPAI-1 (p=0.78), or resistin (p=0.91). The association was not confounded by BMI, parity, age at first full-term birth, age at menopause, current postmenopausal hormone use, and circulating sex steroid hormones. Furthermore, adipokine associations were not modified by BMI (p>0.05). The lack of association with risk may be due to measurement error of the laboratory assays. DISCUSSION: lower levels of adiponectin and higher levels of aPAI-1 measured in prospectively-collected serum from postmenopausal women were associated with increasing BMI but not breast cancer risk.
INTRODUCTION:Obesity is a well-established risk factor for postmenopausal breast cancer, but mechanisms underlying the association are unclear. Adipocyte-derived, cytokine-like adipokines have been suggested as contributory factors. To evaluate their association with breast cancer risk factors and breast cancer risk, we conducted a nested case-control study of 234 postmenopausal breast cancer cases and 234 controls in a cohort of U.S. women with prospectively-collected serum samples obtained in the mid 1970s and followed for up to 25 years. METHODS:Adiponectin, absolute plasminogen activator inhibitor-1 (aPAI-1), and resistin were measured by a multiplex immunoassay. Sex hormones were available for 67 cases and 67 controls. RESULTS: Among controls, we found that lower levels of adiponectin and higher levels of aPAI-1 were correlated with increasing levels of estradiol (Spearman r=-0.26, p-value=0.033; r=0.42, p=0.0003), decreasing levels of sex hormone binding globulin (r=0.38, p=0.0013; r=-0.32, p=0.0076), and increasing body mass index (BMI) (r=-0.31, p=<0.0001; r=0.39, p=<0.0001). Hormones were not associated with resistin. Among the relatively small percentage of women using postmenopausal hormones at the time of blood collection (13.7%), aPAI-1 levels were higher than in non-users (p=0.0054). Breast cancer risk was not associated with circulating levels of adiponectin (age-adjusted p for linear trend=0.43), aPAI-1 (p=0.78), or resistin (p=0.91). The association was not confounded by BMI, parity, age at first full-term birth, age at menopause, current postmenopausal hormone use, and circulating sex steroid hormones. Furthermore, adipokine associations were not modified by BMI (p>0.05). The lack of association with risk may be due to measurement error of the laboratory assays. DISCUSSION: lower levels of adiponectin and higher levels of aPAI-1 measured in prospectively-collected serum from postmenopausal women were associated with increasing BMI but not breast cancer risk.
Authors: J F Dorgan; F Z Stanczyk; C Longcope; H E Stephenson; L Chang; R Miller; C Franz; R T Falk; L Kahle Journal: Cancer Epidemiol Biomarkers Prev Date: 1997-03 Impact factor: 4.254
Authors: J F Dorgan; C Longcope; H E Stephenson; R T Falk; R Miller; C Franz; L Kahle; W S Campbell; J A Tangrea; A Schatzkin Journal: Cancer Epidemiol Biomarkers Prev Date: 1996-07 Impact factor: 4.254
Authors: Maxime P Look; Wim L J van Putten; Michael J Duffy; Nadia Harbeck; Ib Jarle Christensen; Christoph Thomssen; Ronald Kates; Frédérique Spyratos; Mårten Fernö; Serenella Eppenberger-Castori; C G J Fred Sweep; Kurt Ulm; Jean-Philippe Peyrat; Pierre-Marie Martin; Henri Magdelenat; Nils Brünner; Catherine Duggan; Björn W Lisboa; Pär-Ola Bendahl; Véronique Quillien; Alain Daver; Gabriel Ricolleau; Marion E Meijer-van Gelder; Peggy Manders; W Edward Fiets; Marinus A Blankenstein; Philippe Broët; Sylvie Romain; Günter Daxenbichler; Gudrun Windbichler; Tanja Cufer; Simona Borstnar; Willy Kueng; Louk V A M Beex; Jan G M Klijn; Niall O'Higgins; Urs Eppenberger; Fritz Jänicke; Manfred Schmitt; John A Foekens Journal: J Natl Cancer Inst Date: 2002-01-16 Impact factor: 13.506
Authors: I Mertens; M Van der Planken; B Corthouts; M Wauters; F Peiffer; I De Leeuw; L Van Gaal Journal: Horm Metab Res Date: 2001-10 Impact factor: 2.936
Authors: Mia M Gaudet; Alpa V Patel; Lauren R Teras; Juzhong Sun; Peter T Campbell; Victoria L Stevens; Eric J Jacobs; Susan M Gapstur Journal: Int J Mol Epidemiol Genet Date: 2013-09-12
Authors: Nicholas J Ollberding; Yeonju Kim; Yurii B Shvetsov; Lynne R Wilkens; Adrian A Franke; Robert V Cooney; Gertraud Maskarinec; Brenda Y Hernandez; Brian E Henderson; Loïc Le Marchand; Laurence N Kolonel; Marc T Goodman Journal: Cancer Prev Res (Phila) Date: 2013-03
Authors: Henry J Thompson; Scot M Sedlacek; Pamela Wolfe; Devchand Paul; Susan G Lakoski; Mary C Playdon; John N McGinley; Shawna B Matthews Journal: Nutrients Date: 2015-06-26 Impact factor: 5.717