surveillance. STAT5a expression has been studied closely in prostate and breast cancer, and has only recently shown some promise with colorectal and head and neck cancer. Unphosphorylated or inactive STAT5a may suppress tumor growth in colorectal cancer and active STAT5a expression in premalignant and tumor lesions has shown potential as a prognostic marker in oral squamous cell carcinoma. Prostate Cancer STAT5a is involved in the maintenance of integrated prostate epithelial structure and has been shown to be critical for cell viability and tumor growth. Stat5a/b is persistently active in prostate cancer cells and inhibition of STAT5a/b has resulted in large scale apoptotic death, although the specific role of STAT5a and distribution of activity remains largely unknown. Prolactin has been known to activate the JAK2-STAT5a/b pathway in both normal and malignant prostate epithelium, but again, the specific activity of STAT5a remains unknown. Breast Cancer In normal tissue, STAT5a mediates effects of prolactin in mammary glands. In breast cancer, STAT5a signaling is important for maintain tumor differentiation and suppressing disease progression. Studies originally showed a correlation between high STAT5a expression and tumor differentiation in mice models, but histopathological analysis of human breast cancer tissue has shown a different trend. It was shown that low nuclear levels of STAT5a was associated with unfavorable clinical outcomes and cancer progression independent of STAT5b expression. High STAT5a was suggested to be an inhibitor of invasion and metastasis and therefore an indicator of favorable clinical outcomes. Because of these trends, it has been proposed as a predictor of response to therapies such as anti-estrogen treatment. Therapeutic Treatment Approaches Because the specific activity of STAT5a has not been extensively investigated, most potential therapeutic treatments aim to target STAT5a/b. So far, the only reported potential therapeutic benefit specific to STAT5a has been in colorectal cancer. Inhibition of STAT5a alone would not effect colorectal cancer cells, but when combined with chemotherapies such as cisplatin, it could increase the chemosensitivity of the cancer cells to the drugs. Therapy schemes currently focus on STAT5a/b, targeting and inhibiting different mediators of the JAK2-STAT5 pathway. Interactions STAT5A has been shown to interact with: CRKL, Epidermal growth factor receptor, ERBB4, Erythropoietin receptor, Janus kinase 1, Janus kinase 2, MAPK1 NMI, and PTPN11. CBX5, See also STAT5 References Further reading Transcription factors