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the more so as the degree of malignancy increases (Anaplasia refers to the more primitive undifferentiated state of the constituent cells) However, it is currently thought that many tumors arise from more primitive elements, speci cally stem cells, and it may be that the ostensible dedifferentiation is an artifact of the histologic appearance of tumors The factor of age is also important in the biology of brain tumors Medulloblastomas, polar spongioblastomas, optic nerve gliomas, and pinealomas occur mainly before the age of 20 years, and meningiomas and glioblastomas are most frequent in the sixth decade Heredity gures importantly in the genesis of certain tumors, particularly retinoblastomas, neuro bromas, and hemangioblastomas The rare familial disorders of multiple endocrine neoplasia and multiple hamartomas are associated with an increased incidence of anterior pituitary tumors and meningiomas, respectively Glioblastomas and cerebral astrocytomas have also been reported occasionally in more than one member of a family, but the study of such families has not disclosed the operation of an identi able genetic factor Only in the gliomas associated with neuro bromatosis and tuberous sclerosis and in the cerebellar hemangioblastoma of von Hippel-Lindau is there signi cant evidence of a hereditary determinant Although there is no direct evidence for an association between viruses and primary tumors of the nervous system, epidemiologic and experimental data drawn from studies of the human papillomavirus and the hepatitis B, Epstein-Barr, and human T-lymphotropic viruses indicate that they may be a risk factor in certain human cancers In transgenic mice, certain viruses are capable of inducing olfactory neuroblastomas and neuro bromas Each of these viruses possesses a small number of genes that are incorporated in a cellular component of the nervous system (usually a dividing cell such as an astrocyte, oligodendrocyte, ependymocyte, endothelial cell, or lymphocyte) The virus is believed to thrive on the high levels of nucleotides and amino acid precursors and at the same time acts to force the cell from of its normal reproductive cycle into an unrestrained replicative cycle (Levine) Because of this capacity to transform the cellular genome, the virus product is called an oncogene; such oncogenes are capable of immortalizing, so to speak, the stimulated cell to form a tumor Molecular and Genetic Features of Brain Tumors All of the above ideas have been expanded greatly by studies of the human genome, which have led to the identi cation of certain chromosomal aberrations linked to tumors of the nervous system What has emerged from these studies is the view that the biogenesis and progression of brain tumors are a consequence of defects in the control of the cell cycle Some molecular defects predispose to tumor genesis; others underlie subsequent progression and accelerated malignant transformation In effect, this model presupposes the acquisition of multiple defects over time In some instances, the initial predisposition is a genetic defect that is inherited by germline transmission and that the additional events arise as somatic genetic lesions For example, mutations in genes that normally suppress cell proliferation may set the stage for tumor development Typically, these inherited mutations affect only one of two copies of the tumor suppressor or gene By itself, such a mutation does not cause cancer However, if the second copy of the gene acquires a mutation (eg, from a chemical toxin or irradiation), the tumor suppression function of the gene is lost and cancerous transformation of the cell becomes likely These notions are consistent with the observation that many of the gene defects that predispose to cancer are dominantly inherited.

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The above model is well illustrated by consideration of the astrocytoma Among the rst detectable changes are mutations that inactivate the tumor suppressor gene, p53 on chromosome 17p; over 50 percent of astrocytomas have deletions encompassing this gene Other early changes include overexpression of growth factors or their receptors as noted below After the tumor develops, progression to a more malignant grade of astrocytoma or to a glioblastoma may be triggered by defects in the p16-retinoblastoma gene signaling pathway, loss of chromosome 10 (seen in about 90 percent of high-grade gliomas), or overexpression of the epidermal growth factor gene In fact, it is striking that analysis of the patterns of these defects correlates accurately with the staging and aggressive characteristics of these tumors Knowledge of the molecular signatures of certain other tumors has immense clinical value For example, as discussed further on, oligodendrogliomas that have combined deletions in chromosomes 1p and 19q respond well to chemotherapy, and this property may increase survival by more than 10 years This type of information may spare the nonresponsive patient from ineffective, sometimes toxic therapy (see Reifenberger and Louis; Louis et al) Much of the modern genetic classi cation of brain tumors is derived from the technical tour de force of gene microarrays The patterns of these multiple gene analyses are able to distinguish some types of medulloblastomas from the similar-appearing primitive neuroectodermal tumors; the medulloblastomas express classes of genes that are characteristic of cerebellar granule cells, suggesting they arise from these cells Also, these gene expression signatures confer useful prognostic information in a more general way than noted above for oligodendroglioma For example, medulloblastomas that express genes indicative of cerebellar differentiation are associated with longer survival than those expressing genes related to cell division (Pomeroy et al) Furthermore, as alluded to earlier, in about 50 percent of gliomas there is an overexpression or a mutant form of epidermal growth factor (EGF) and of transforming growth factor alpha (TGF- ), suggesting a role for these in the progression of certain tumor types Other trophic factors are overexpressed in yet other brain neoplasms and perhaps contribute to their morphology and growth pattern; for example, VEGF is found in extremely high concentrations in meningiomas, which are highly vascular by nature These ndings, taken together, suggest an autocrine stimulation of growth by these factors and possibly an interaction with some of the aforementioned gene defects However, having emphasized molecular and chromosomal changes, it is not yet clear if any of them is truly causative (the currently favored hypothesis) or if they simply re ect an aberrant genetic process that accompanies the dedifferentiation of tumor growth and progression On the basis of this new molecular information, our views of the pathogenesis of neoplasia are being cast along new lines Some of the speci cs of these new data are presented in the following discussions of particular tumor types A more extensive review can be found in the article by Osborne and colleagues, including the heterogeneity of ndings that suggests polygenic changes in most gliomas.

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Now we turn our attention to the WAD templates With the WAD templates, we encounter another approach to the migration process In this case, we have a migration wizard, shown next, to help us through the steps