Robert H. Lurie Comprehensive Cancer Center, Department of Medicine-Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, 300 E Superior Street-Tarry 13-705, Chicago, IL 60611, USA.
Immunotherapy. 2014;6(1):19-21. doi: 10.2217/imt.13.154.
Evaluation of: Beavis PA, Divisekera U, Paget C et al. Blockade of A2A receptors potently suppresses the metastasis of CD73(+) tumors. Proc. Natl Acad. Sci. USA 110(36), 14711-14716 (2013). CD73 is becoming an emerging therapeutic target for the prevention of tumor growth and metastasis. However, the mechanism by which CD73 promotes tumor metastasis is unclear. Beavis et al. evaluated the efficacy of A2A and A2B adenosine receptor antagonists in inhibiting the metastasis of tumors expressing CD73, either endogenously or ectopically. They demonstrate distinct mechanisms whereby A2A versus A2B adenosine receptors could contribute to CD73(+) tumor metastasis. As A2Areceptor (R)/A2BR antagonists have been tested in clinical trials in other disease settings, this study highlights the potential therapeutic application of an A2AR/A2BR blockade strategy for treatment of CD73(+) metastatic tumors.
Beavis PA、Divisekera U、Paget C 等人。A2A 受体阻断剂有力抑制 CD73(+)肿瘤的转移。Proc. Natl Acad. Sci. USA 110(36), 14711-14716 (2013)。CD73 正成为预防肿瘤生长和转移的新兴治疗靶点。然而，CD73 促进肿瘤转移的机制尚不清楚。Beavis 等人评估了 A2A 和 A2B 腺苷受体拮抗剂在抑制内源性或外源性表达 CD73 的肿瘤转移中的疗效。他们证明了 A2A 与 A2B 腺苷受体通过不同的机制有助于 CD73(+)肿瘤转移。由于 A2A 受体（R）/A2BR 拮抗剂已在其他疾病治疗的临床试验中进行了测试，因此该研究强调了 A2AR/A2BR 阻断策略在治疗 CD73(+)转移性肿瘤方面的潜在治疗应用。
