BIOLOGICAL HETEROGENEITY OF GLIOMAS

Specific recurring chromosomal and genetic alterations have been ident ified in gliomas, forming a model of tumor progression from benign gli oma to glioblastoma multiforme. However, the heterogeneity of glioma m olecular changes seems to reflect the variety of clinical outcomes cha racterizing these tumors. Loss of genetic material on chromosomes 17, 9 and 19 has been associated with glioma pathogenesis, while changes i n chromosome 10 may indicate a poor prognosis. Gliomas also express gr owth factors (GF) and GF receptors that may be important in promoting tumor growth, e.g., epidermal GF, fibroblast GF and vascular endotheli al GF. Tumor invasion, also a glioma feature, may involve proteases su ch as plasminogen activator (PA) and metalloproteases, under the regul ation of specific receptors and inhibitors. PA inhibitor type 1, assoc iated with the most aggressive form of glioma, may also contribute to tumor neoangiogenesis. Description and understanding of these alterati ons may help to develop new modalities of glioma therapy.