Fueyo J, Gómez-Manzano C
Departamento de Neurooncología, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
Neurologia. 1998 Aug-Sep;13(7):349-55.
Cancer represents perhaps the most formidable challenge in medicine and science in general. Currently, gliomas are one of the most deadly cancers. Despite aggressive therapy using surgery, radiotherapy and chemotherapy, the prognosis of glioma patients is very poor. The design of new therapies for these tumors is therefore mandatory. Molecular medicine is based on the discovery of fundamental molecular components that determine normal cellular behavior, and are aberrant in cancer cells, and in the subsequent exploitation of these new uncovered targets to generate specific and nontoxic treatments for cancer. In addition with the activation or amplification of oncogenes, progressive inactivation of tumor suppressor genes is one of the characteristics of the malignant progression of gliomas. One of the most promising approaches of gene therapy is the transfer of such tumor suppressor genes to cancer cells. In gliomas, p53, p16 and Rb abnormalities are present in the vast majority of gliomas. Restoration of the wild-type functions of these genes results in either apoptosis or suppression of glioma growth with very low toxicity. This review highlights a small sample of areas where conceptual and practical advances in molecular biology are changing our understanding of the pathogenesis of these tumors.
癌症或许是整个医学和科学界面临的最严峻挑战。目前，胶质瘤是最致命的癌症之一。尽管采用了手术、放疗和化疗等积极治疗方法，但胶质瘤患者的预后仍然很差。因此，必须为这些肿瘤设计新的治疗方法。分子医学基于对决定正常细胞行为且在癌细胞中异常的基本分子成分的发现，以及随后对这些新发现靶点的利用，以产生针对癌症的特异性且无毒的治疗方法。除了癌基因的激活或扩增外，肿瘤抑制基因的逐渐失活是胶质瘤恶性进展的特征之一。基因治疗最有前景的方法之一是将此类肿瘤抑制基因转移到癌细胞中。在胶质瘤中，绝大多数胶质瘤都存在p53、p16和Rb异常。恢复这些基因的野生型功能会导致细胞凋亡或抑制胶质瘤生长，且毒性极低。本综述重点介绍了分子生物学在概念和实践方面的进展正在改变我们对这些肿瘤发病机制理解的一小部分领域。
