Okamura K
Department of Neurosurgery, Toyohashi Municipal Hospital.
Nihon Rinsho. 1995 Nov;53(11):2678-83.
Recent advances in molecular genetics have disclosed oncogenes playing a significant role in the development of malignant gliomas. Amplification of the c-erb gene which code EGFR and aberration of P53 oncogene play a significant role in the development of most malignant gliomas. Karyotype analysis of malignant gliomas revealed gains of chromosome 7, loss of chromosome 10, double minutes and loss of heterozygosity. The development of the tumors appear to result from the accumulation of those multiple genetic alterations. Although many cases of familiar malignant gliomas have been reported the role of hereditary factors in familial transmission still remains controversial. Chromosomal abnormalities seemed to be confined to the tumor cell, and no alteration in karyotype of peripheral blood, which indicated germ line mutation, was demonstrated. However, several authors indicated that the frequency of malignant gliomas in the relatives of patients was estimated more than ten times to the controls. Some hereditary factors might play a role in malignant gliomas.
分子遗传学的最新进展揭示了癌基因在恶性胶质瘤发展中发挥着重要作用。编码表皮生长因子受体（EGFR）的c-erb基因的扩增以及P53癌基因的畸变在大多数恶性胶质瘤的发展中起着重要作用。恶性胶质瘤的核型分析显示7号染色体增加、10号染色体缺失、双微体以及杂合性缺失。肿瘤的发生似乎是由这些多种基因改变的积累所致。尽管已经报道了许多家族性恶性胶质瘤病例，但遗传因素在家族性传播中的作用仍存在争议。染色体异常似乎局限于肿瘤细胞，未显示外周血细胞的核型改变，这表明不存在种系突变。然而，几位作者指出，患者亲属中恶性胶质瘤的发生率估计比对照组高出十多倍。一些遗传因素可能在恶性胶质瘤中起作用。
