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Genetic modeling of glioma formation in mice.

机译:小鼠神经胶质瘤形成的遗传模型。

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摘要

In addition to the histological features that define gliomas, mutations and other alterations in gene expression and signal transduction are classically found in these tumors. Some of these alterations are likely to be the effects of the neoplastic phenotype, while others may be causative agents essential to the etiologic origin of the disease. The determination of whether specific genetic alterations, either individually or in combination, can serve as the etiology of gliomas requires modeling in animals with the fulfillment of Koch's postulates. Animal modeling studies not only provide information on the potential causes of glioma formation, they also identify novel candidate targets for therapy and provide tumor-bearing animals for preclinical trials. Recently, remarkable strides have been made in the generation of mouse models of the diffuse gliomas that provide unparalleled opportunities for advancing our knowledge of the etiology, maintenance, and treatment of this lethal class of tumors.
机译:除了定义神经胶质瘤的组织学特征外,经典地在这些肿瘤中发现了基因表达和信号转导中的突变和其他改变。这些改变中的某些可能是肿瘤表型的影响,而另一些则可能是该病的病因起源所必需的病原体。确定特定的遗传改变(无论是单独还是组合)是否可以作为神经胶质瘤的病因,需要在动物中模拟科赫的假设。动物模型研究不仅提供了有关神经胶质瘤形成的潜在原因的信息,还确定了治疗的新候选靶点,并为临床前试验提供了荷瘤动物。最近,弥漫性神经胶质瘤的小鼠模型的开发已取得了长足的进步,这些模型为增进我们对这种致死性肿瘤的病因学,维持和治疗的认识提供了无与伦比的机会。

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