Genetic predisposition to cancer with special reference to mutagen sensitivity

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Abstract
From studies on cancer genetics, available information suggests the following tentative conclusions: Cancer starts with a genetic change (or changes) from a normal somatic cell, but the changes (mutational events) must be specific in a target tissue cell. In a number of cases, genetic changes can be detected at the chromosome level. Hereditary cancers usually have one genetic lesion already existing prezygotically; therefore only one additional mutational event is required in the homologous gene to complete the process of neoplastic transformation. In nonhereditary neoplasms, both mutations must occur postzygotically. Individuals with high spontaneous mutation rates (monitored by chromosome breakage rates) are more liable to acquire specific genetic lesions than those with low mutation rates; therefore they are at higher risk to develop neoplasms. Individuals with genetic defects in response to damage induced by mutagens (carcinogens) are more liable to accumulate genetic lesions than those who are more resistant; therefore, they are more liable to develop cancers. Mutagen sensitivity or resistance is probably genetic expression of DNA repair capabilities. An effective assay method for sensitivity or resistance to mutagens can be developed to analyze the human population to identify the at-risk fraction.