Metabolic Populational in vivo Construction of Tumors under Conditions of Individual Genetic Predisposition: Communication II

Abstract

The results of the analysis of the literature data on the ethnic distribution of xenobiotic biotransformation phenotypes and on tumor incidence (for all organs in total) are presented from the standpoint of the concept by L.A. Piruzyan [1]. For a number of ethnic groups, a possibility is theoretically shown of the metabolic populational in vivo construction of tumors (depending on the genetically determined metabolic status of certain populations), i.e., of the ethnic dependence of tumors. In the American population, the higher incidence of the slow acetylation phenotype than in Swedes and in the Chinese was associated with the higher incidence of morbidity. In populations of the English, the Germans, the Swedes, and the Swiss, characterized by a low incidence of the slow acetylation phenotype, the tumor morbidity was higher than in the Chinese with a higher incidence of slow acetylators. Americans are more predisposed to tumors than the Swedes. Caucasoids with either the slow or the fast acetylation phenotype are more predisposed to tumors than the Chinese. The prevalence of the fast acetylation phenotype in the Chinese and Japanese populations was associated with the lower cancer morbidity: in the Chinese compared to Australians, Danes, Swedes; in the Japanese compared to Australians, Americans, the English, Danes, Canadians, the German, the Portuguese, Finns, Czechs, and Slovaks. The lower incidence of the slow acetylators in the Chinese than in Americans, English, Danes, Canadians, Germans, Finns, Czechs, Slovaks, and Swedes was associated with a lower rate of morbidity. In the Portuguese, the higher incidence of fast acetylators than in Danes and the lower incidence of slow acetylators than in Czechs, Slovaks, and Afro-Americans was associated with the lower rate of morbidity. In the Hong Kong and Singapore Chinese with the lower incidence of slow acetylators than in the Madras Negroids, the morbidity was higher. In Australians and Swedes, the greater fraction of slow acetylators was associated with a lower morbidity than in Afro-Americans. In the Russian population of St. Petersburg, the higher incidence of slow acetylators was associated with the lower morbidity compared to the Hong Kong Chinese. Among Poles, the slow acetylator incidence was higher and the morbidity was lower than in the Portuguese. The Japanese and the Chinese (fast acetylators) are less predisposed to cancer than the above-listed Caucasoids; among Caucasoids, the Portuguese (fast acetylators) were less predisposed to cancer than the Danes, Czechs, Slovaks, and Afro-Americans. The tumor predisposition of the Hong Kong and Singapore Chinese was higher than the predisposition of the Madras Negroids. Australians, Russians (St. Petersburg residents), and Poles were less predisposed to cancer than Afro-Americans, the Hong Kong Chinese, and the Portuguese. The morbidity of the Madras Negroids with the higher incidence of the slow acetylation phenotype was lower than the morbidity of the Hong Kong and Singapore Chinese. The incidence of the slow acetylation phenotype in Afro-Americans was lower than in the Australians and Swedes and higher than in the Portuguese, Chinese, and Japanese; this was associated with the higher cancer morbidity, i.e., with the increased predisposition to tumors. The lower incidence of the T1-0 phenotype of glutathione-S-transferase in the English than in the Singapore and Shanghai Chinese and in the Japanese was associated with the higher morbidity of the English. In the Singapore Chinese, the higher incidence of the M1-0 and of T1-0 phenotypes of glutathione-S-transferase than in the Japanese was associated with the increased morbidity. In some populations, different morbidities were associated with similar incidences of one or another metabolic phenotype, or different phenotype incidences in different populations were associated with similar morbidities. The morbidity under consideration did not include chemical carcinogenesis, i.e., the conversion of procarcinogens to true carcinogens or the carcinogen inactivation. Because the results presented are preliminary, this article outlines the directions of theoretical studies that are required for definite conclusions concerning the ethnic dependence of tumors.