有丝分裂检查点激活时间延长在癌症形成和治疗中的作用。
Role of prolonged mitotic checkpoint activation in the formation and treatment of cancer.
机构信息
Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
出版信息
Future Oncol. 2009 Nov;5(9):1363-70. doi: 10.2217/fon.09.118.
Abstract
Mitotic abnormalities are a common feature of human cancer cells, and recent studies have provided evidence that such abnormalities may play a causative, rather than merely incidental role, in tumorigenesis. One such abnormality is prolonged activation of the mitotic checkpoint, which can be provoked by a number of the gene changes that drive tumor formation. At the same time, antimitotic chemotherapeutics exert their clinical efficacy through the large-scale induction of prolonged mitotic checkpoint activation, indicating that mitotic arrest is influential in both the formation and treatment of human cancer. However, how this influence occurs is not well understood. In this perspective, we will discuss the current evidence in support of the potential mechanisms by which prolonged activation of the mitotic checkpoint affects both tumorigenesis and antimitotic chemotherapy.
摘要
有丝分裂异常是人类癌细胞的一个常见特征，最近的研究提供了证据表明，这种异常可能在肿瘤发生中起因果作用，而不仅仅是偶然作用。有丝分裂检查点的持续激活就是这样一种异常，它可以由许多驱动肿瘤形成的基因变化引发。与此同时，抗有丝分裂的化疗药物通过大规模诱导有丝分裂检查点的持续激活来发挥其临床疗效，这表明有丝分裂阻滞对人类癌症的形成和治疗都有影响。然而，这种影响是如何发生的还不是很清楚。在这篇观点文章中，我们将讨论目前支持有丝分裂检查点持续激活影响肿瘤发生和抗有丝分裂化疗的潜在机制的证据。
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