By Alfred G. Knudson Jr. (auth.), Harry Harris, Kurt Hirschhorn (eds.)
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Extra resources for Advances in Human Genetics 8
Age, a patient's probability of having a tumor in a particular tissue would be a function of the mean number of tumors observed in a population of individuals carrying the MEA 1 mutation. Different members of the same family might have very different clinical expressions, depending on the sites of the somatic mutations. The hyperplasia might, on the other hand, be an expression of the inherited mutation itself and affect most or all of the cells in a tissue. 273 This condition is dominantly inherited.
S. Blacks, a low rate among Mrican Blacks, and a low rate among Japanese in Japan, with an increase among Japanese immigrants to the United States317 These differences are evidently not genetic. It is of great interest, however, that incidentally found, latent, noninvasive carcinoma of the prostate has approximately the same age-corrected incidence in Whites and Japanese. The study of families has shown that an increased genetic risk occurs for this cancer, but it is not suggestive of Mendelian predisposition.
156 This hypothesis has not been adequately tested, although in one instance there was a translocation between chromosomes 8 and 11, with a small deletion of the former. 237 In one family, a mother with hemihypertrophy but no tumor had three children with Wilms' tumor but no hemihypertrophy. 208 Another condition characterized by abnormal growth and predisposition to Wilms' tumor is the Beckwith-Wiedemann syndrome. 247 Genitourinary anomalies are also observed with increased frequency in Wilms' tumor patients,237 the incidence being higher in bilateral cases.