Abstract
Family studies provide one of the best means for investigating genetic environmental interactions in cancer etiology. Environmental differences may be compared between the members of high risk families (i.e., those with remarkably high familial cancer frequencies) who have developed the disease and those who have not. The establishment of constitutional markers to identify those individuals who are particularly at risk for the familial cancer may profoundly enhance the significance of such studies. Different types of cancers are sometimes aggregated in the same kindred. The existence of familial aggregations of these disease entities suggests the involvement of an underlying etiological unity to them. Studies of cancer genetics at the infrahuman level have had the advantage of controlled experimentation, the lack of which is obvious and poses a serious deterrent in human studies. Thus, the development of highly inbred strains of animals has made it possible to evaluate the genotype of the host with a high degree of precision. In turn, the role of environment and its interactions with the genotype has made it possible to evaluate the exigencies of this interplay with a high degree of accuracy. In certain well designed animal experiments, it is now possible to draw conclusions for a genetic hypothesis for cancer etiology; namely, one can evaluate the relative roles of genetics and environment in carcinogenesis. The general conclusion stemming from numerous studies of this nature, i.e., wherein genetic and extragenetic factors can be controlled, has been that the individual's genotype plays a major role in response to carcinogens; thus, it is obviously mandatory that carcinogenic factors be evaluated critically in their relationship and/or interaction with host factors.