Triple negative breast cancer (TNBC), defined by lack ER, PR and HER2 expression, currently poses clinical problems due to lack of targeted therapies. Androgen is one of the leading candidates in the search for effective therapies of TNBC patients but the biological functions of AR have still remained unclear as disparate finding reported in the literature. While previous studies have shown that AR can be associated with a lower proliferation in invasive ductal carcinoma (IDC), at least in clinical specimens, it is not clear  whether AR regulation of cell proliferation may influence disease development. Therefore, in order to further evaluate the relationship between AR and tumour cell proliferation we examined TNBC ductal in situ carcinomas (DCIS).  Following IRB approval cohort of DCIS, the specimens were retrieved from two Japanese hospitals (Tohoku Kosai Hospital Sendai Japan and St Lukes Hospital Tokyo, n=42). Immunoreactivity of AR and Ki-67 was evaluated by H score and labelling index respectively. When comparing Ki-67 labelling index between AR positive and negative DCIS cases, the positive AR status was significantly associated with a lower Ki67 labelling index (p=<.001; Pos(>10% AR LI): 19.4±12.8; Neg(<10% AR LI) : 61.1±7.2).  AR immunoreactivity was also greater in DCIS compared to historical IDC data (DCIS: 80% positive, H Score 73.3±6.2; IDC n=87: 35% positive, H score 28.7±4.3, p<0.001). The Ki-67 LI associated with AR positivity was not significantly different between DCIS and historical IDC (DCIS 19.4±12.8, IDC 25.8±22.6). Results of our present study clearly demonstrated a linkage between the loss of AR between DCIS and IDC and the AR loss clearly resulted in subsequent increase in carcinoma cell proliferation. The loss of AR and subsequent loss of suppression of proliferation could be involved in the transition from TNBS DCIS to IDC.