The past few years have seen remarkable progress in understanding the
molecular genetic basis of glioma formation. Affected oncogenes and tu
mor suppressor genes have been identified and putative tumor suppresso
r loci have been mapped. These studies have illustrated distinct molec
ular pathways for different glial neoplasms. We summarize the findings
of an ongoing study initiated to characterize human gliomas on a mole
cular basis. The data are compiled from 150 astrocytic, oligodendrogli
al, and mixed gliomas that were assessed for genomic alterations chara
cteristic of these neoplasms, i.e., loss of portions of chromosomes 1p
, 9p, 10, 17p, 17q, and 19q, mutations of the p53 tumor suppressor gen
e, and amplification of the EGF receptor (EGFR) gene. Our findings sup
port the hypothesis that distinct genetic pathways result in the forma
tion of astrocytic and oligodendroglial neoplasms of different maligna
ncy grades, and that glioblastoma multiforme may be subdivided into ge
netically distinct subsets, Such findings may not only lead to a bette
r understanding of neoplastic transformation in glial cells, but may a
lso have a major impact on clinical neuro-oncology. (C) 1995 Wiley-Lis
s, Inc.