MBC remained an extremely rare disease. Although less frequent, it tended to be more aggressive than its female counterpart 
. Most of our current knowledge regarding its biology, natural history and treatment strategies had been extrapolated from its female counterpart. Estrogen and progesterone were thought to play an important role in development and progression of breast cancer in women. However, the role of androgen in breast cancer etiology was poorly understood. Wang 
found better survival in ER-positive MBC patients but did not find a benefit from treatment with Tamoxifen. More recently, Pich 
found no correlation between the expression of ER or PR with overall survival. They concluded that MBC patients are biologically different from female breast carcinoma (FBC) patients and questioned the rationale for the use of anti-hormonal (Tamoxifen) therapy in MBC patients. Much research was needed to characterize further the molecular biological properties of MBC and their prognostic significance, and to devise treatment strategies, including optimal endocrine regimens. In our study, AR-positive expression was detected in 82.7% of MBC patients; this rate was identical with that reported (81%) by Noman Kidwai 
and similar to the rate of 74% observed by Pich 
. Moreover, AR protein expression was related to ER and PR protein expression in our study. Analogous other studies on FBCs or MBCs, we found a correlation between AR and ER or PR status 
. This correlation mechanism will require us to continue to study in MBC.
The role of AR expression as a prognostic factor was controversial. In MBC, Pich 
showed lack of association between AR and survival, whereas Munoz 
suggested that decreased androgen action (AR-negative) within the breast might contribute to an earlier development of MBC. In contrast, we found a strong correlation between AR protein expression and survival (5y-OS and 5y-DFS) in MBC patients. AR-positivity was associated with adverse prognosis and AR status had prognostic significance in univariate analysis. The similar findings 
together with our results might indicate a new opinion of endocrine therapy (anti androgenic therapy) for MBC patients.
The involvement of AR in MBC development had been also investigated at the DNA level 
. AR activity could be affected by the highly variable polyglutamine tract (CAG repeat) located in the NH2-terminal trans activation domain of the AR. Expansion of the CAG repeat had been associated with reduced AR expression/transactivation, whereas the relatively short CAG repeat sequence increased the level of transactivation of the AR 
. Interestingly, in our study long CAG repeat sequence was associated with increased AR expression appeared in the tumor tissue and the rate was 90%. This phenomenon was worthy of our further research. Furthermore, we should continue to explore and discover the regulatory factor of the nucleic acid to protein transcription and inhibit this regulatory factor which might inhibit tumor development and metastasis.
We initiated to test CAG repeat length of blood and tumor tissue in the same MBC patient. Interestingly, the test results of two paired samples were the same in each patient. As the incidence of MBC was low, the size of our study cohort was small. Although there were only 31 MBC patients who had paired samples, these consistent results supported two paired samples information substituted for one another. We had observed statistically significant difference between the CAG repeat length of MBC patients and controls. In addition, no males in the control group had alleles containing more than 28 CAG repeats. Only one of the MBC patients had an allele containing 14 repeats, compared to 6 of the controls. The length of this CAG repeat had been investigated in several studies of MBC patients and controls previously 
. Our study was consistent with the Australian study 
that found statistically significant difference in CAG repeat length between MBC patients and controls. To our knowledge, there were no data on prognostic value of AR (CAG)n repeats status in MBC. However, it was found to be significantly different survival between long and short CAG repeat sequence in MBC patients. We believed that a relatively long CAG repeat sequence within the AR gene might be implicated in a few cases of MBC and poor prognosis. Conversely, a short CAG repeat sequence might offer a degree of protection against male breast cancer.
This study revealed the following important findings: (a) there was a significant difference in the CAG repeat lengths between MBC patients and controls; (b) long CAG repeat lengths were more common in patients than controls and there was a strong trend toward short CAG repeat lengths being more prevalent in controls than in cases; (c) long CAG repeat sequence presented at the T2-4 stage compared with short CAG repeat sequence in MBC patients but did not differ with respect to other clinicopathological features; (d) there was a significant difference by ER and PR status regarding AR expression in the MBC patients; (e) the presence of long CAG repeat sequence and AR-positive expression were associated with shorter survival of MBC patients.
To conclude, the findings presented in this study indicate that the CAG repeat length within the AR gene might be one useful molecular biomarker to identify males at increased risk of breast cancer development. The CAG repeat length and AR expression were two independent prognostic indicators in MBC patients. Larger studies were required to define the importance of AR (CAG)n repeats status and AR expression in MBC further and we had agreed to contribute our data to this.