Advances in Human Genetics 8 by Alfred G. Knudson Jr. (auth.), Harry Harris, Kurt Hirschhorn

By Alfred G. Knudson Jr. (auth.), Harry Harris, Kurt Hirschhorn (eds.)

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213 Conceivably, there is even a common pathway in the generation of teratomas. The tumor phenotype may depend on some somatic change, such as alteration or failure of appearance of a specific surface macromolecule, which in tum could be a consequence of mutation of a gene (gonadal and some extragonadal cases in man) or of interference with expression of a gene (other extragonadal cases). MUTATION AND HUMAN CANCER A Mutation Model and the Incidence of Cancer Since the early statements of Boveri and Tyzzer on the origin of cancer by somatic mutation, a considerable body of new data has been brought to bear on the hypothesis.

Similarly, one mutation might account Chapter 1: Genetics and Etiology of Human Cancer 41 for ovarian teratoid tumors, there being too few data to decide whether dysgerminoma should be included as a possible outcome. A third mutation concerns sacrococcygeal teratomas, as it does not overlap with either of the above mutations. Frontonasal and intracranial teratomas appear to be attributable to a fourth mutant. This sum of four different mutations is obviously a minimum. The target cells for these mutations are apparently different.

258 The tendency for gliomas and medulloblastomas to be isolated from each other within pedigrees suggests that the genetic predisposition has some specificity with respect to level of differentiation as well as affected organ. Similarly, the occurrence of elements of Chapter 1: Genetics and Etiology of Human Cancer 33 both glioma and medulloblastoma within a tumor is very rare, although it has been reported. 254 On the other hand, a variant of medulloblastoma, "medullomyoblastoma," contains both neuroectodermal and mesenchymal elements, suggesting a relationship to teratoma.

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