There are reports in the literature of families in which a very high proportion of the members are affected with retinoblastoma. This suggests some factor other than the action of a simple autosomal gene (Fig. 1, Griffith and Sorsby1; Fig. 2, Wilson, cited by Bell2).
In 1954 Reese stated that he had seen only one survivor of retinoblastoma with healthy children. At that time 77% of the collected offspring of survivors were affected.3 This high percentage does not conform to the usual pattern for dominant traits, which characteristically produce 50% affected offspring when one parent is genotypically normal and the other is heterozygous.
One flaw in the report of Dr. Reese is his method of obtaining family trees from affected children. This immediately weighs the scale in favor of high incidence of affected children. The data were derived from 15 families, each with one parent who had
MANCHESTER PT. Retinoblastoma Among Offspring of Adult Survivors. Arch Ophthalmol. 1961;65(4):546–549. doi:10.1001/archopht.1961.01840020548015
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