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• W115378045 abstract "DURING the past few decades, experimental oncology has described both the multiplicity and the vast spectrum of agents which can, under the appropriate conditions, induce tumor formation and the heterogeneous biological and biochemical alterations which occur in the resultant tumors. In very general terms, carcinogenesis can be described as a series of changes that occur in a when it is exposed to the appropriate stimulus and result in the phenotypic traits which characterize a tumor. In a given experiment, both the pattern of phenotypic changes occurring during carcinogenesis and the life history of the resultant tumor are unique. Although this is generally true, and indeed each tumor seen clinically has unique characteristics, nevertheless a of biological and enzymatic characteristics occurs during carcinogenesis. Thus, arising from different tissues tend to loise their specialized characteristics and become more similar to one another than to the tissues from which they originated. Based on enzyme analyses of a number of tumors, Greenstein formulated the convergence hypothesis oif cancer in which he concluded that tumors tend to converge enzymatically to a common type of tissue (1). A number of different agents or conditions may effectuate the carcinogenic transformation-the DNA and RNA viruses; radiation of different types; chemical agents including literally thousands of different types and structures; films of metals, plastic, or glass; hormonal stress of the appropriate severity; and, finally, normal cells become malignant when they are simply propagated in culture in vitro. The multiplicity and heterogeneity of causal agents clearly indicate that the initial cellular sites of action of the carcinogen in each case ma,y be quite different. However, the of biological and enzymatic character during carcinogenesis suggests that these agents are affecting common cellular mechanisms. This iis suggested by other data, as well; thus, carcinogens may act either synergistically or antagonistically. A good example of this is the well-known promoting or inhibiting activities of certain hormones on chemical carcinogenesis (2, 3). Another interesting example is the synergism between X-radiation and the carcinogen urethan in experimental leukemogenesis (4). Although the diversity of carcinogenic agents implies that there is no single, common, initial The authors are with the Etiology Area, National Cancer Institute, Public Health Service." @default.
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• W115378045 title "Genetic Regulatory Mechanisms and Carcinogenesis" @default.
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• W115378045 doi "https://doi.org/10.2307/4592834" @default.
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