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Differences in Risk Factors for Breast Cancer Molecular Subtypes in a Population-Based Study

Xiaohong R. Yang¹, Mark E. Sherman¹, David L. Rimm³, Jolanta Lissowska⁴, Louise A. Brinton¹, Beata Peplonska⁶, Stephen M. Hewitt², William F. Anderson¹, Neonila Szeszenia-Dbrowska⁶, Alicja Bardin-Mikolajczak⁴, Witold Zatonski⁴, Richard Cartun⁹, Daniza Mandich⁹, Grzegorz Rymkiewicz⁵, Marcin Ligaj⁵, Stanislaw Lukaszek⁸, Radzisaw Kordek⁷ and Montserrat García-Closas¹

¹ Division of Cancer Epidemiology and Genetics, ² Tissue Array Research Program, Laboratory of Pathology, Center For Cancer Research, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland; ³ Department of Pathology, Yale University School of Medicine, New Haven, Connecticut; ⁴ Department of Cancer Epidemiology and Prevention, and ⁵ Department of Pathology, Cancer Center and M. Sklodowska-Curie Institute of Oncology, Warsaw, Poland; ⁶ Department of Occupational andEnvironmental Epidemiology, Nofer Institute of Occupational Medicine, ⁷ Department of Pathology, Medical University of ód; ⁸ Department of Clinical Pathomorphology, Polish Mother's Memorial Hospital-Research Institute, ód, Poland; and ⁹ Department of Pathology, Hartford Hospital, Hartford, Connecticut

Requests for reprints: Xiaohong Yang, Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Room 7014, 6120 Executive Boulevard, Bethesda, MD 20892-7236. Phone: 301-594-7804; Fax: 301-402-4489. E-mail: royang{at}mail.nih.gov

Analysis of gene expression data suggests that breast cancers are divisible into molecular subtypes which have distinct clinical features. This study evaluates whether pathologic features and etiologic associations differ among molecular subtypes. We evaluated 804 women with invasive breast cancers and 2,502 controls participating in a Polish Breast Cancer Study. Immunohistochemical stains for estrogen receptor , progesterone receptor, human epidermal growth factor receptors (HER2 and HER1), and cytokeratin 5 were used to classify cases into five molecular subtypes: luminal A, luminal B, HER2-expresing, basal-like, and unclassified. Relative risks were estimated using adjusted odds ratios and 95% confidence intervals. We observed that compared with the predominant luminal A tumors (69%), other subtypes were associated with unfavorable clinical features at diagnosis, especially HER2-expressing (8%) and basal-like (12%) tumors. Increasing body mass index significantly reduced the risk of luminal A tumors among premenopausal women (odds ratios, 0.71; 95% confidence intervals, 0.57-0.88 per five-unit increase), whereas it did not reduce risk for basal-like tumors (1.18; 0.86-1.64; P_{heterogeneity} = 0.003). On the other hand, reduced risk associated with increasing age at menarche was stronger for basal-like (0.78; 0.68-0.89 per 2-year increase) than luminal A tumors (0.90; 0.95-1.08; P_{heterogeneity} = 0.0009). Although family history increased risk for all subtypes (except for unclassified tumors), the magnitude of the relative risk was highest for basal-like tumors. Results from this study have shown that breast cancer risk factors may vary by molecular subtypes identified in expression studies, suggesting etiologic, in addition to clinical, heterogeneity of breast cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(3):439–43)

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