Abstract 249: Dietary supplementation with methylseleninic acid reduces male mammary tumorigenesis in MMTV-PyMT mice

Abstract

Abstract Male breast cancer makes up approximately 1% of all breast cancers and less than 1% of all cancers in men in the United States. However, it is an aggressive disease with poor prognosis and the incidence of male breast cancer is on the rise. The present study investigated the effects of dietary supplementation of selenium on male breast carcinogenesis in MMTV-PyMT mice (FVB/N background). Three-week-old male mice were weaned onto the AIN93G diet with or without supplementation of selenium in the form of methylseleninic acid (2.5 mg Se/kg). Mice were euthanized 10 weeks after the first palpable mammary tumor was detected. There were no differences in food intake and body weight between the groups. The median latency (the age at which the first palpable tumor was detected) was 14.1 and 13.9 weeks and the incidence of palpable mammary tumor was 71% and 70% for the control and the selenium group, respectively. Selenium supplementation compared to the control diet reduced mammary tumor progression by 258% and tumor weight by 84%, respectively. Tumor progression was defined as the change in tumor volume from detection of the first palpable mammary tumor to termination 10 weeks later. Incidence of lung metastasis was 74% and 50% in control and selenium group, respectively. In mice bearing lung metastases, selenium supplementation significantly reduced the number of metastases by 83% compared to the control group. In conclusion, dietary supplementation with selenium in the form of methylseleninic acid reduces male breast carcinogenesis and its metastasis in mice. It indicates that selenium may be useful in male breast cancer prevention. Citation Format: Sneha Sundaram. Dietary supplementation with methylseleninic acid reduces male mammary tumorigenesis in MMTV-PyMT mice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 249. doi:10.1158/1538-7445.AM2017-249