Background: Molecular data have shown that TNBC was a heterogeneous group of tumors. The objective was to evaluate prognosis of IHC sub-classification adapted from molecular model. Methods: We used IHC sub-classification based on positivity for androgen receptor (AR) (Roche, SP 107), cytokeratine 5/6 (CK) (Dako, D5/16B4) and Epidermal growth factor receptor (EGFR) (Biosd, 31G7). Samples with more than 10% AR nuclear immunostaining were considered positive. Threshold for CK and EGFR was 1%. We distinguished 4 groups of tumors: AR phenotype (AR+, EGFR-, CK5/6-), basal-like phenotype (AR-, EGFR+/-, CK5/6 +/-), triple-negative phenotype (AR-, EGFR-, CK5/6-) and mixed group (AR+, EGFR+/-, CK5/6 +/-). Tissue micro-array blocks were constructed with samples from a retrospective cohort treated in adjuvant setting for non metastatic TNBC in a single institution from 2003 to 2013. Survival data were estimated by the Kaplan-Meier method and compared by the log-rank test in univariate analysis. Multivariate analysis including tumor size (T), lymph nodes status (N) and lymphovascular invasion (LVI) was performed using Cox model. Results: 105 patients were followed-up for a median period of 56.3 months [6-155]. Median age was 54 years [29-80]. 57.1% were stage pT1, 41.9% were pN+ and 37,1% presented LVI. 11 patients were classified as AR phenotype, 35 as basal-like, 46 as triple-negative phenotype and 13 as mixed group. 18 patients developed metastases: 3/11 AR, 5/35 basal-like, 6/46 triple-negative and 4/13 mixed group. No difference was observed between TNBC subgroups in terms of disease free survival DFS (p = .98) and overall survival OS (p = .86). T, N and LVI were the only prognostic factors (p = .05, p = .05 and p = .046 respectively). Conclusions: We found no impact of IHC sub-classification of TNBC. Correlation between IHC and molecular biology is in progress.