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The genomes of various tumour cells contain mutant oncogenes that act dominantly, in that their effects can be observed when they are introduced into non-malignant cells^1–4. There is evidence for another class of oncogenes, in which tumour-predisposing mutations are recessive to wild-type alleles^5–7. Retinoblastoma is a prototype biological model for the study of such recessive oncogenes⁸. This malignant tumour, which arises in the eyes of children, can be explained as the result of two distinct genetic changes, each causing loss of function of one of the two homologous copies at a single genetic locus, Rb (refs 9–12), assigned to the q14 band of human chromosome 13 (refs 13–22). Mutations affecting this locus may be inherited from a parent, may arise during gametogenesis or may occur somatically. Those who inherit a mutant allele at this locus have a high incidence of non-ocular, second tumours²³ …