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for reasons elaborated further on Tumors derived from the choroid plexus are divided into two classes papillomas and carcinomas, both rare Meningiomas are classi ed on the basis of their cytoarchitecture and genetic origin into four catergories: the usual meningothelial or syncytial type, the broblastic and angioblastic variants, and the malignant type Tumors of the pineal gland, which were not included in earlier classi cations, comprise germ-cell tumors, the rare pineocytomas, and pineoblastomas The medulloblastoma has been reclassi ed with other tumors of presumed neuroectodermal origin, namely neuroblastoma, retinoblastoma, and ependymoblastoma Given separate status also are the intracranial midline germcell tumors, such as germinoma, teratoma, choriocarcinoma, and endodermal sinus carcinoma A miscellaneous group comprises large-cell reticular lymphoma (CNS lymphoma), hemangioblastoma, chordoma, hemangiopericytoma, spongioblastoma, and ganglioneuroma Tumors of cranial and peripheral nerves are believed to differentiate into three main types: schwannomas, neuro bromas, and neuro brosarcomas Biology of Nervous System Tumors In considering the biology of primary nervous system tumors, one of the rst problems is with the de nition of neoplasia It is well known that a number of lesions may simulate brain tumors in their clinical manifestations and histologic appearance but are really hamartomas and not true tumors A hamartoma is a tumor-like formation that has its basis in maldevelopment (Russell) and undergoes little change during the life of the host The dif culty one encounters in distinguishing it from a true neoplasm, whose constituent cells multiply without restraint, is well illustrated by tuberous sclerosis and von Recklinghausen neuro bromatosis, where both hamartomas and neoplasms are found In a number of mass lesions such as certain cerebellar astrocytomas, bipolar astrocytomas of the pons and optic nerves, von Hippel-Lindau cerebellar cysts, and pineal teratomas a clear distinction between neoplasms and hamartomas is often not possible The many studies of the pathogenesis of brain tumors have gradually shed light on their origin Johannes Muller (1838), in his atlas Structure and Function of Neoplasms, rst enunciated the appealing idea that tumors might originate in embryonic cells left in the brain during development This idea was elaborated by Cohnheim (1878), who postulated that the source of tumors was an anomaly of the embryonic anlage Ribbert, in 1918, extended this hypothesis by postulating that the potential for differentiation of these stem cells would favor blastomatous growth This CohnheimRibbert theory seems most applicable to tumors that arise from vestigial tissues, such as craniopharyngiomas, teratomas, lipomas, and chordomas, some of which are more like hamartomas than neoplasms For many years, thinking about the pathogenesis of primary CNS tumors was dominated by the histogenetic theory of Bailey and Cushing (1926), which is based on the known or assumed embryology of nerve and glial cells Although it is not a popular notion today, Bailey and Cushing attached the suf x blastoma to indicate all tumors composed of primitive-looking cells such as glioblastoma and medulloblastoma One prominent theory is that most tumors arise from neoplastic transformation of mature adult cells (dedifferentiation) A normal astrocyte, oligodendrocyte, microgliocyte, or ependymocyte is transformed into a neoplastic cell and, as it multiplies, the daughter cells become variably anaplastic,
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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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