曼徹斯特大學(the University of Manchester)的研究團隊研發(fā)了一個新的化學藥物能夠抑制Aurora B的活性,，在細胞的試驗中證明能有效的毒殺癌細胞,。
Stephen Taylor博士說：「其實最初是Aurora A被作為抗癌標靶的酵素，也由此促成了Aurora B的發(fā)現(xiàn),，而且毒殺癌細胞的效果比Aurora A更好,。」此研究發(fā)表于近期的Cell Science期刊,，也引起了全世界抗癌團隊對Aurora抑制物的好奇,，目前有超過 10家制藥公司努力的在探索Aurora抗癌的計劃。
雖然抑制Aurora A也看得到潛在的治療效果,，但是這份研究很清楚的顯示Aurora B有急起直追的潛力,，早期的臨床試驗已證明Aurora B并沒有顯著的毒性及副作用,，這個結果將有利于Aurora B在短時間內進入下一階段的臨床試驗。許多現(xiàn)有的抗癌藥雖然效果很好,，但卻有毒副作用,，而Aurora的優(yōu)勢就是其幾乎沒有毒副作用，因此未來應可成為一個革命性的抗癌新藥,。
Aurora A以及Aurora B是一種蛋白質激酶(protein kinase),，它們會將其它的蛋白質磷酸化，引發(fā)訊息傳遞誘導癌細胞生長,。曼徹斯特研究團隊與制藥公司AstraZeneca共同研發(fā)Aurora B抑制物,，早在2003年就指出以Aurora B作為抗癌標靶深具潛力，而最近的實驗結果驗證了Aurora B抑制物確實能有效的用于癌癥治療,。
部分英文原文：
Validating Aurora B as an anti-cancer drug target
The Aurora kinases, a family of mitotic regulators, have received much attention as potential targets for novel anti-cancer therapeutics. Several Aurora kinase inhibitors have been described including ZM447439, which prevents chromosome alignment, spindle checkpoint function and cytokinesis. Subsequently, ZM447439-treated cells exit mitosis without dividing and lose viability. Because ZM447439 inhibits both Aurora A and B, we set out to determine which phenotypes are due to inhibition of which kinase. Using molecular genetic approaches, we show that inhibition of Aurora B kinase activity phenocopies ZM447439. Furthermore, a novel ZM compound, which is 100 times more selective for Aurora B over Aurora A in vitro, induces identical phenotypes. Importantly, inhibition of Aurora B kinase activity induces a penetrant anti-proliferative phenotype, indicating that Aurora B is an attractive anti-cancer drug target. Using molecular genetic and chemical-genetic approaches, we also probe the role of Aurora A kinase activity. We show that simultaneous repression of Aurora A plus induction of a catalytic mutant induces a monopolar phenotype. Consistently, another novel ZM-related inhibitor, which is 20 times as potent against Aurora A compared with ZM447439, induces a monopolar phenotype. Expression of a drug-resistant Aurora A mutant reverts this phenotype, demonstrating that Aurora A kinase activity is required for spindle bipolarity in human cells. Because small molecule-mediated inhibition of Aurora A and Aurora B yields distinct phenotypes, our observations indicate that the Auroras may present two avenues for anti-cancer drug discovery.
