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Cure of Glioma: A Space Not Yet Occupied for the Lesion

In the United States, there are approximately 17,000 cases of primary central nervous system malignant neoplasms diagnosed per year, accounting for about 2% of cancers. Approximately 13,000 deaths occur per year in this country that are caused by primary central nervous systemic tumors. Of these primary central nervous system malignancies approximately 60% are gliomas, and the majority of these—roughly 65%—are high grade—that is, Grade III (termed Anaplastic Astrocytoma) and Grade IV (termed Glioblastoma Multiforme). These malignancies derive from neuroglial cells, the connective tissue matrix cells that provide architectural support for neurons and respond to brain injury. There are several grading systems. The most prominent is the World Health Organization Grading System, but the Kernohan and Sayre system, the Daumas-Dupont system, and the Saint Ann Mayo system are also used. These systems rely upon several factors, including tumor cellularity, numbers of mitoses, nuclear atypia, endothelial proliferation, and necrosis within the tumor; the greater the degree of any of these findings, particularly necrosis, the higher the grade of the tumor, and the worse the prognosis. Median survival has been poor for these diseases; for Glioblastoma Multiforme, despite multimodality therapy, the median survival is in the range of nine to 12 months, with two-year survival rates in the range of 8% to 12%. However, even for patients with low-grade astrocytoma managed aggressively, the survival is in the range of only 50% to 60% at five years from diagnosis. In recent years, there have been advances in the understanding of the pathobiology of gliomas, including the identification of some of the molecular changes which occur. Mutations in the p53 tumor suppressor gene are frequent, with partial or complete loss of its locus on chromosome 17p, as is true of many cancers. Mutations in the Retinoblastoma gene, with abnormalities involving the Rb gene locus on chromosome 13q, and mutations in CDKn2a with deletions at chromosome 9p have also been observed. Other abnormalities have been seen in other proto-oncogene sites, including the gene coding for Platelet Derived Growth Factor, Epidermal Growth Factor Receptor, and CDK4. However, none of these mutations are unique to gliomas, and much remains to be understood regarding the progression of genetic lesions that give rise to gliomas. These issues have been reviewed recently. Attempts to improve survival of patients through advances in therapeutics have been equally vexing. We know that for high grade lesions, ‘‘complete’’ surgical excision is associated with improved survival, as compared to incomplete surgical excision. Radiotherapy following surgery is well accepted, and has