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Molecular genetic analysis of non‐astrocytic gliomas

Gliomas are the most common primary tumours of adult central nervous system with major subtypes of astrocytoma, oligodendroglioma and ependymoma. However, the classifications of gliomas and effective therapies remain controversial and elusive. In recent years, glioma has come under intense investigation to understand the molecular basis of tumorigenesis. It is well known now that tumorigenesis involves alterations in oncogenes and tumour suppressor genes resulting in activation and inactivation, respectively, and leading to the cells becoming immortalized, proliferating, invading and modulating their environment. The molecular genetic studies of common gliomas implicate epidermal growth factor and its receptor, platelet-derived growth factor and its receptors, as common oncogenes, and genes on chromosome 1p, 9p, 10, 13q, 17p, 19q and 22q as tumour suppressor genes. The molecular events responsible for astrocytoma (most common subtype of glioma) formation and progression have been clarified more than other types of glioma. It is also now possible to correlate these alterations with specific histological and biological features of astrocytoma (grade II), anaplastic astrocytoma (grade III) and glioblastoma multiforme (grade IV). In astrocytomas, it is thought that p53 mutation plus platelet-derived growth factor and its receptor overexpression plus loss of a gene in 22q are responsible for the formation of astrocytoma. From there, the mutation of Rb gene on 13q, and loss of tumour suppressor genes on 9p and 19q would lead to anaplastic astrocytoma. The abnormality in chromosome 10, particularly the loss of tumour suppressor gene on 10p and 10q, in addition to the amplification of epidermal growth factor, are responsible for the transformation of anaplastic astrocytoma to glioblastoma multiforme. The oligodendrogliomas and ependymomas are less frequent than astrocytomas. The cytogenetic analysis of these two tumours has lagged far behind studies done on astrocytoma. In oligodendroglioma, oncogene amplification for instance has only rarely been noted. Most reports indicate that chromosomal loss may involve, preferentially, chromosomes 1p and 19q. These two abnormalities may be responsible for formation of oligodendroglioma, while loss of 10p and 10q, in addition to the epidermal growth factor receptor amplification, are responsible for transformation of oligodendroglioma to the anaplastic oligodendroglioma and ultimately to glioblastoma multiforme. In a recent report by Maintz et al. it was suggested that two genetic subsets of oligoastrocytoma (which is a tumour mixed between oligodendroglioma and astrocytoma) exist, one genetically related to astrocytoma and the other genetically related to oligodendroglioma. Histologically, those oligoastrocytomas with p53 mutation were more often astrocytoma-predominant, while those with chromosome 19q loss were more often oligodendroglioma predominant. Similarly, for ependymoma, only few reported studies have targeted the molecular biology of ependymoma which highlighted the need for further investigation into the factors that may provide the elusive key to prognosis in ependymoma. It appeared that ependymoma has a complex genetic abnormality; 30% show abnormality of chromosome 22 (independent of NF2 gene); abnormalities of 9p, 10, 17p and 13q chromosomes are less common in ependymoma than in high-grade astrocytoma. Anaplastic ependymoma is only slightly more likely to have abnormal karyotypes than benign ependymoma. Therefore, it is thought that the loss of 22q would be a crucial factor in ependymoma while possibly loss of 10p and 10q and other unknown factors are responsible for the transformation of ependymoma to anaplastic ependymoma. The role of growth factors in oncogenesis and prognosis needs to be established in ependymoma in addition to the prognostic value of tumour suppressor genes like p53 and 22q. It is important to remember that the assumption that all gliomas progress in a linear fashion through distinct genetic stages is an over-simplification because each glioma does not show all the described genetic changes Histopathology 1999, 34, 370–371