25-Hydroxy vitamin-D, obesity, and associated variables as predictors of breast cancer risk and tamoxifen benefit in NSABP-P1

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• 作者：Eitan Amir (1)
  Reena S. Cecchini (2)
  Patricia A. Ganz (3)
  Joseph P. Costantino (24)
  Samantha Beddows (5)
  Nicola Hood (5)
  Pamela J. Goodwin (15) pgoodwin@mtsinai.on.ca
• 关键词：Breast cancer &#8211 ; Vitamin ; D &#8211 ; Obesity &#8211 ; Cancer prevention &#8211 ; Tamoxifen
• 刊名：Breast Cancer Research and Treatment
• 出版年：2012
• 出版时间：June 2012
• 年：2012
• 卷：133
• 期：3
• 页码：1077-1088
• 全文大小：526.5 KB
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• 作者单位：1. Division of Medical Oncology and Hematology, Princess Margaret Hospital and University of Toronto, Toronto, ON, Canada2. Biostatistical Center, National Surgical Adjuvant Breast and Bowel Project, Pittsburgh, PA, USA3. Los Angeles Schools of Medicine and Public Health, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA4. Department of Biostatistics, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, USA5. Department of Medicine, Mount Sinai Hospital and University of Toronto, 1284-600 University Ave, Toronto, ON M5G 1X5, Canada
• ISSN：1573-7217

文摘

Observational studies suggest that host factors are associated with breast cancer risk. The influence of obesity, vitamin-D status, insulin resistance, inflammation, and elevated adipocytokines in women at high risk of breast cancer is unknown. The NSABP-P1 trial population was used for a nested case&#8211;control study. Cases were drawn from those who developed invasive breast cancer and controls selected from unaffected participants (≤4 per case) matched for age, race, 5 year Gail score, and geographic location of clinical center as a surrogate for latitude. Fasting serum banked at trial enrolment was assayed for 25-hydroxy vitamin-D (25OHD), insulin, leptin (adipocytokine), and C-reactive protein (CRP, marker of inflammation). Logistic regression was used to test for associations between study variables and the risk of invasive breast cancer. Two hundred and thirty-one cases were matched with 856 controls. Mean age was 54, and 49% were premenopausal. There were negative correlations for 25OHD with body mass index (BMI), insulin, CRP, and leptin. BMI ≥ 25 kg/m2 was associated with higher breast cancer risk (odds ratio [OR] 1.45, p = 0.02) and tamoxifen treatment was associated with lower risk (OR = 0.44, p < 0.001). Suboptimal 25OHD (<72 nmol/l) did not influence breast cancer risk (OR = 1.06, p = 0.76). When evaluated as continuous variables, 25OHD, insulin, CRP, and leptin levels were not associated with breast cancer risk (all p > 0.34). In this high risk population, higher BMI was associated with a greater breast cancer risk. Serum levels of 25OHD, insulin, CRP, and leptin were not independent predictors of either breast cancer risk or tamoxifen benefit.