Furnari F B, Huang H J, Cavenee W K
Ludwig Institute for Cancer Research, University of California San Diego, La Jolla 92093-0660, USA.
Cancer Surv. 1995;25:233-75.
Progression of gliomas to more malignant phenotypes involves numerous molecular genetic alterations. The genes affected by these alterations, the steps in malignant progression for which they are responsible, their normal function in controlling diverse cellular functions such as differentiation, signal transduction, cell cycle progression and angiogenesis and how they may act in concert with other tumour suppressor genes or oncogenes are some of the questions finally coming into focus and being studied. As other genes are discovered, their association with tumour progression can be assessed, coupled with current histopathology and used to determine more accurately patient prognosis and strategies for intervention. With the generation of specific reagents, such as monoclonal antibodies directed to glioma derived antigens or emerging gene therapy techniques designed to deliver toxic, antisense or reconstituting genes specifically to tumour tissue, new approaches will be devised that may finally be used to treat these tumours effectively.
胶质瘤向更恶性表型的进展涉及众多分子遗传学改变。这些改变所影响的基因、它们在恶性进展中所负责的步骤、它们在控制诸如分化、信号转导、细胞周期进程和血管生成等多种细胞功能中的正常功能,以及它们如何与其他肿瘤抑制基因或癌基因协同作用,是一些最终开始受到关注并正在研究的问题。随着其他基因的发现,可以评估它们与肿瘤进展的关联,并结合当前的组织病理学,用于更准确地确定患者的预后和干预策略。随着特异性试剂的产生,如针对胶质瘤衍生抗原的单克隆抗体或旨在将毒性、反义或重组基因特异性递送至肿瘤组织的新兴基因治疗技术,将设计出新的方法,最终可能用于有效治疗这些肿瘤。