Familial and sporadic human renal cell carcinoma : evidence against a double-loss mechanism of carcinogenesis.
It has been speculated that renal cell carcinoma (RCC) is an example of a double-loss mutation.
We analyzed the age distribution of 71 cases of familial RCC and of 11 population-based cancer registries [German Democratic Republic, Denmark, Finland, Norway, Sweden, U.S.A. Whites, U.S.A. Blacks, Miyagi and Osaka Prefectures (Japan), Hong Kong, and Israeli Jews] according to the multi-hit and clonal growth models of carcinogenesis.
The analysis rules out a double-loss mechanism for RCC.
On both of the two models analyzed, carcinogenesis in the familial cases of RCC arises as a result of a three-to ten-fold increase in the average rate of mutation at the susceptible loci, as compared with the sporadic cases.
In general, the clonal growth model provides a somewhat better fit to the age-distribution of RCC incidence than does the multi-hit model.
Mots-clés Pascal : Epithélioma, Rein, Homme, Etude familiale, Epidémiologie, Age, Modèle mathématique, Incidence, Mutation, Sporadique, Maladie héréditaire, Etude comparative, Carcinogenèse, Tumeur maligne, Rein pathologie, Appareil urinaire pathologie
Mots-clés Pascal anglais : Carcinoma, Kidney, Human, Family study, Epidemiology, Age, Mathematical model, Incidence, Mutation, Sporadic, Genetic disease, Comparative study, Carcinogenesis, Malignant tumor, Renal disease, Urinary system disease
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Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 95-0382480
Code Inist : 002B14D01. Création : 01/03/1996.