Histone hyperacetylation affects G2/M cell cycle transition

在癌症中，控制细胞生长的机制经常被破坏。我们已经确定了这种增长控制机制。当正常的体细胞用一种被称为组蛋白去乙酰化酶抑制剂的特殊药物治疗时，它们的反应是停止增殖，但当药物被移除时，它们会恢复正常生长。然而，我们发现类似治疗的肿瘤细胞被这些药物杀死。正常细胞和肿瘤细胞之间的区别在于特定生长控制的功能。确定这种生长控制机制如何在正常细胞中运作，并确定肿瘤细胞中的缺陷，有可能为更特异性和更有效的抗癌药物确定新的靶点。增加的特异性，即只破坏肿瘤细胞，而对周围的正常身体组织几乎没有影响，将是非常有益的，因为传统抗癌治疗的缺点之一是它们有害的正常组织毒性。这是与化疗和放疗相关的许多使人衰弱的副作用的原因，这些副作用可能限制这些治疗的临床效果。

The mechanisms controlling cell growth are often disrupted in cancers. We have identified on such growth control mechanism. When normal body cells are treated with a particular family of drugs known as histone deacetylase inhibitors, they react by stopping proliferating, but will resume normal growth when the drug is removed. However, we have found that similarly treated tumour cells are killed by these drugs. The difference between the normal and tumour cells is the functionality of a particular growth control. The identification of how this growth control mechanism operates in normal cells, and defining the defect in tumour cells has the potential to identify new targets for more specific and potent anti-cancer drugs. The increased specificity, i.e. destruction of only the tumour cells while have little or no effect on the surround normal body tissue, would be extremely beneficial as one of the drawbacks to conventional anti-cancer treatments is their unwanted normal tissue toxicities. This is cause of the many debilitating side effects associated with chemo and radiotherapy which can limit the clinical effectiveness of these treatments.