As the emergence of cancer is most frequent in proliferating tissues, replication errors are considered to be at the base of this disease. This review concentrates mainly on two neural cancers, neuroblastoma and glioma, with completely different backgrounds that are well documented with respect to their ontogeny. Although clinical data on other cancers of the nervous system are available, usually little can be said about their origins. Neuroblastoma is initiated in the embryo at a moment when the nervous system (NS) is in full expansion and occasionally genomic damage can lead to neoplasia. Glioma, to the contrary, occurs in the adult brain supposed to be mostly in a postmitotic state. According to current consensus, neural stem cells located in the subventricular zone (SVZ) in the adult are thought to accumulate enough genomic mutations to diverge on a carcinogenic course leading to diverse forms of glioma. After weighing the pros and cons of this current hypothesis in this review, it will be argued that this may be improbable, yielding to the original old concept of glial origin of glioma. 1. The Origins of Neural Cancers Several hypotheses on the origin of cancers in general and those of the nervous system in particular have been proposed in the last century [1]. Currently, most hypotheses are based on the idea that a cancer is the result of the accumulation of several mutations, estimated at about 6 [2]. For this accumulation to occur, the precancer cell must be a cell that divides regularly such as those that form the nervous system during embryogenesis. Neuroblastoma is a childhood cancer of the nervous system in which the N-myc protooncogene transcription factor (N-myc) is often overexpressed [3]. This transcription factor is essential during neurogenesis for the rapid expansion of progenitor cell populations. It is encoded by the neuroblastoma-derived myelocytomatosis oncogene (MYCN). Overexpression of MYCN in transgenic mice indeed causes neuroblastoma in their pups [4]. It has been speculated that glioma and glioblastoma might arise from astrocytes with appropriate genetic abnormalities because astrocytes and their progenitors were, for long, the only cell types known to be capable of replication in the adult NS [5–7]. Expression of a mutated, constitutively active, epidermal growth factor receptor (EGFR) gene in mice brain causes glioblastoma-like lesions [8] and infection with the viral oncogene v-ERB, a homologue of EGFR, initiates oligodendroglioma in mice [9]. Glial tumours are generally of a heterogeneous composition, containing cells
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