De novoglioblastomas develop in older patients without prior clinical history of less malignant tumors. Progressive glioblastomas are common among younger patients and arise through progression from lower-grade astrocytomas.CDKN2Adeletions,PTENalterations, andEGFRamplification are more prevalent amongde novoglioblastomas, whereas p53 mutations are more common among progressive glioblastomas. Loss of heterozygosity (LOH) for chromosome 10 is seen uniformly among bothde novoand progressive high-grade astrocytomas. The inactivation of thePTENgene is found in approximately 30% to 40% of astrocytomas with chromosome 10 loss, and LOH pattern in the remaining astrocytomas strongly supports the presence of another yet unidentified tumor suppressor gene telomeric toPTEN.More than 80% of oligodendrogliomas exhibit LOH for 1p and 19q alleles. Oligoastrocytomas with 1p/19q LOH are related to oligodendrogliomas, and those with p53 mutations are related to astrocytomas.