[Biological profiles of malignant gliomas].
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.
Chinot
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Laboratoire de Cancérologie Expérimentale, CJF INSERM 93-11, Faculté de Médecine Secteur Nord, Marseille, France.
D002869:Chromosome Aberrations / Q000235:genetics*; D025063:Chromosome Disorders; D004815:Epidermal Growth Factor / Q000235:genetics*; D066246:ErbB Receptors / Q000235:genetics*; D005910:Glioma / Q000235:genetics* / Q000473:pathology; D006801:Humans; D009361:Neoplasm Invasiveness; D011494:Protein Kinases / Q000235:genetics; D012697:Serine Endopeptidases / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
D016159:Tumor Suppressor Protein p53; D004815:Epidermal Growth Factor; D011494:Protein Kinases; D066246:ErbB Receptors; D012697:Serine Endopeptidases
Profils biologiques des gliomes malins.