Mutagenesis and embryonal carcinogenesis.
The embryonal tumors of children occur in dominantly heritable and nonhereditary forms, which indicates that a dominant mutation can be on the carcinogenic pathway. A model which fits age-specific incidence hypothesizes that both forms arise as a consequence of two mutations. The background incidences of these tumors then reflect spontaneous mutation rates in germinal and somatic cells and may be increased by mutagens. The gene for one tumor (retinoblastoma) seems to be located on chromosome 13. Clues to the pathophysiology of these tumor genes come from consideration of their tissue specificity, origin from embryonal cells, and developmental effects. Childhood cancers may be manifestations of the homozygous states of a series of genes concerned with differentiation in specific embryonal tissues.
D002648:Child; D002869:Chromosome Aberrations; D002901:Chromosomes, Human, 13-15; D005134:Eye Neoplasms / Q000235:genetics; D005260:Female; D005799:Genes, Dominant; D006801:Humans; D007668:Kidney / Q000002:abnormalities; D007680:Kidney Neoplasms / Q000235:genetics; D008954:Models, Biological; D009154:Mutation; D009373:Neoplasms, Germ Cell and Embryonal / Q000235:genetics*; D009378:Neoplasms, Multiple Primary / Q000235:genetics; D009928:Organ Specificity; D011247:Pregnancy; D012175:Retinoblastoma / Q000235:genetics; D009396:Wilms Tumor / Q000235:genetics