Research Article Promoter Methylation Status of Breast Cancer Susceptibility Gene 1 and 17 Beta Hydroxysteroid Dehydrogenase Type 1 Gene in Sporadic Breast Cancer Patients Marwa M. Hosny, 1 Nagwan A. Sabek, 1 Taghrid B. El-Abaseri, 1 Fathalla M. Hassan, 1 and Sherif H. Farrag 2 1 Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Suez Canal University, Round Road, Ismailia 41111, Egypt 2 Surgery Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt Correspondence should be addressed to Nagwan A. Sabek; nagwan yasser@yahoo.com Received 11 December 2015; Revised 6 February 2016; Accepted 29 February 2016 Academic Editor: Claudio Luparello Copyright © 2016 Marwa M. Hosny et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Epigenetic modiications are involved in breast carcinogenesis. Identifying genes that are epigenetically silenced via methylation could select target patients for diagnostic as well as therapeutic potential. We assessed promoter methylation of breast cancer susceptibility gene 1 (BRCA1) and 17 Beta Hydroxysteroid Dehydrogenase Type 1 (17HSD-1) in normal and cancer breast tissues of forty sporadic breast cancer (BC) cases using restriction enzyme based methylation-speciic PCR (REMS-PCR). In cancerous tissues, BRCA1 and 17HSD-1 were methylated in 42.5% and 97.5%, respectively, while normal tissues had 35% and 95% methylation, respectively. BRCA1 methylation in normal tissues was 12.2-fold more likely to associate with methylation in cancer tissues ( < 0.001). It correlated signiicantly with increased age at menopause, mitosis, the negative status of Her2, and the molecular subtype “luminal A” ( = 0.048,  = 0.042,  = 0.007, and  = 0.049, resp.). Methylation of BRCA1 and 17HSD-1 related to luminal A subtype of breast cancer. Since a small proportion of normal breast epithelial cells had BRCA1 methylation, our preliminary indings suggest that methylation of BRCA1 may be involved in breast tumors initiation and progression; therefore, it could be used as a biomarker for the early detection of sporadic breast cancer. Methylation of 17HSD-1 in normal and cancer tissue could save patients the long term use of adjuvant antiestrogen therapies. 1. Introduction Breast cancer is a malignancy arising from the epithelial tis- sues that line the terminal ductal-lobular units of the breast [1, 2]. Breast cancer (BC) is the most common cancer in females worldwide [3]; BC is the leading cause of cancer death among females, with an estimated 1.7 million cases and 521,900 deaths in 2012; BC alone accounts for 25% of all cancer cases and 15% of all cancer deaths among females [4]. Based on data from the National Cancer Registry Program of Egypt (NCRP) in 2008–2011, BC is the most common malignancy among Egyptian females. It constituted 32.0% of all cancer cases [5]. According to GLOBOCAN 2012, the age-standardized incidence rate (ASR) of breast cancer was 42.3 per 100,000 Egyptian females, with a mortality rate of 17.4 per 100,000 females [4]. Many environmental factors combined with multiple genetic and epigenetic changes are involved in the onset and development of breast cancer [6, 7]. he carcinogenesis process is a multistep process during which genetic and epi- genetic alterations accumulate in a cell, resulting in the pro- gressive transformation of normal cells through steps of ini- tiation, promotion, and progression into cancer cells [8]. Epi- genetics are emerging as one of the most important events in carcinogenesis [9]. DNA methylation has an essential role in the regulation of gene expression in mammalian cells [10]. In normal cells, the majority of promoter cytosine phosphate guanosine (CpG) islands are protected from this epigenetic Hindawi Publishing Corporation International Journal of Breast Cancer Volume 2016, Article ID 9545241, 12 pages http://dx.doi.org/10.1155/2016/9545241