Chinot O
Laboratoire de Cancérologie Expérimentale, CJF INSERM 93-11, Faculté de Médecine Secteur Nord, Marseille, France.
Pathol Biol (Paris). 1995 Mar;43(3):224-32.
Specific and recurring chromosomal and genetic alterations have been identified in gliomas and could described a model of tumoral progression from benin glioma to glioblastoma multiforme. However, the heterogeneity of profiles of molecular alterations that have been observed in gliomas seems to reflect the variety of clinical evolutions which characterise those tumors. Loss of genetic material on chromosomes 17, 9 and 19, then of chromosome 10 have been associated to pathogenesis of glioma and a pejorative prognostic value have been attributed to the alteration of chromosome 10. Gliomas also express growth factors and growth factors receptors that may be important in promoting tumor growth, like Epidermal growth factor (EGF), fibroblast growth factors (FGF) and vascular endothelial growth factor (VEGF). Tumoral invasion which characterise also gliomas, may involve proteases like plasminogen activators (PA) and metalloproteases, under the regulation of specific receptors and inhibitors. PA inhibitor type 1 (PAI1), associated to the most aggressive form of gliomas, may also participate to tumoral neoangiogenesis. Description and understanding of these alterations may contribute to develop new treatment modalities in gliomas.
在胶质瘤中已鉴定出特定且反复出现的染色体和基因改变,这些改变可以描述从良性胶质瘤到多形性胶质母细胞瘤的肿瘤进展模型。然而,在胶质瘤中观察到的分子改变谱的异质性似乎反映了这些肿瘤所特有的各种临床演变。17号、9号和19号染色体上的遗传物质丢失,随后10号染色体的丢失与胶质瘤的发病机制有关,并且10号染色体的改变具有不良预后价值。胶质瘤还表达可能在促进肿瘤生长中起重要作用的生长因子和生长因子受体,如表皮生长因子(EGF)、成纤维细胞生长因子(FGF)和血管内皮生长因子(VEGF)。同样表征胶质瘤的肿瘤侵袭可能涉及蛋白酶,如纤溶酶原激活剂(PA)和金属蛋白酶,这受到特定受体和抑制剂的调节。与最具侵袭性的胶质瘤形式相关的1型PA抑制剂(PAI1)也可能参与肿瘤新生血管生成。对这些改变的描述和理解可能有助于开发胶质瘤的新治疗方法。