Our finding that IACs are characterized by an overexpression of HMGCS2, suggests that the patients Amprenavir diagnosed with apocrine carcinoma might benefit from therapy with HMGCS2 inhibitors. In addition, the high levels of AR expression in the IACs makes this receptor a promising anticancer therapeutic target for this type of breast cancer, but the ability to exploit AR for therapy remains to be challenging. Given that AR and HMGCS2 are both overexpressed in IAC, the use of the dual therapy targeting two parallel AR and HMGCS2 pathways may provide an additional benefit for therapeutic Neostigmine Bromide attack of breast apocrine carcinoma. HMGCS2 is the only gene from the breast apocrine protein marker panel identified in our studies that has been included in the molecular apocrine transcriptomic signature, and was also found among the genes which transcription was affected by modulation of AR/FOXA1 axis in apocrine cells. It is plausible, based on these findings, to consider this enzyme as a “marker” to indicate an active AR, which can be used to predict which tumors are driven by this receptor and, therefore, capable of being treated with antiandrogen therapy. To date, there is uncertainty regarding the relationship between molecular apocrine tumors identified by mRNA-array studies and histopatologically�Cdiagnosed apocrine malignancies. Thus, Lehman-Che and co-authors found only 4 tumors that meet morphological criteria for apocrine tumors among 58 patients diagnosed as ����molecular apocrine����, suggesting that molecular apocrine subtype is much broader than initially reported by Farmer and co-authors. Apocrine transcriptomic signatures contain several genes related to signaling pathways, transcription factors and transporters that are not observed in our proteomic signature and therefore were of interest to study. Our reciprocal IHC analysis of a set of 10 proteins selected from the major top candidates of molecular apocrine signature: FOXA1, XBP1, BLVRA, ABCA12, SIDT1, MLPH, RHOB, TSC22D3, SLC2A10 and SLC7A8 has revealed only one protein, melanopholin, an adapter protein involved in melanosome transport to cell periphery, which expression was specific for benign apocrine lesions, but was lost in invasive stages.