MYC is one of the most commonly overexpressed oncogenes in human cancer. The targeted inactivation of MYC is a possible therapy for neoplasia. Conditional transgenic mouse model systems are tractable methods to precisely dissect how and when the inactivation of MYC might be effective in the treatment for human cancer. From these model systems, several general principles emerge. MYC inactivation stereotypically results in the proliferative arrest, differentiation and/or apoptosis of tumor cells. The specific consequences of MYC inactivation appear to depend both on the type of cancer as well as the constellation of genetic events unique to a given tumor. Tumors can escape from dependence upon MYC by acquiring compensatory genetic events. MYC inactivation can uncover the stem cell properties of tumor cells that differentiate into normal appearing cells. In some cases, these differentiated cells are actually dormant tumor cells that recover their neoplastic properties upon MYC reactivation. In other cases, even brief MYC inactivation is sufficient to induce sustained tumor regression. Insights from conditional transgenic mouse models will be useful in the development of therapies that target MYC for the treatment of cancer.

译文

:MYC是人类癌症中最常见的过度表达的癌基因之一。 MYC的靶向失活是一种可能的瘤形成疗法。有条件的转基因小鼠模型系统是精确剖析MYC失活如何以及何时可能有效治疗人类癌症的易处理方法。从这些模型系统中,出现了一些通用原理。 MYC失活定型地导致肿瘤细胞的增殖停滞,分化和/或凋亡。 MYC失活的具体后果似乎取决于癌症的类型以及给定肿瘤特有的遗传事件的构象。肿瘤可以通过获得代偿性遗传事件而摆脱对MYC的依赖。 MYC失活可以揭示分化为正常出现细胞的肿瘤细胞的干细胞特性。在某些情况下,这些分化的细胞实际上是处于休眠状态的肿瘤细胞,它们在MYC激活后会恢复其肿瘤性质。在其他情况下,即使短暂的MYC失活也足以诱导持续的肿瘤消退。来自条件性转基因小鼠模型的见解将有助于开发针对MYC的治疗癌症的疗法。

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