Abstract
Carcinogens show extreme diversity in chemical composition and structure. Since they are almost invariably mutagenic, it is generally assumed that they impart, directly or indirectly, genetic damage which results in the genesis of modified viable or nonviable cells. Viable mutant cells are not necessarily malignant. In fact, some authors believe that cancer cells may be associated with specific chromosomal patterns and that each malignant disease is an expression of a specific karyotype. This hypothesis is attractive in view of the existence of neoplastic diseases that are transmitted in a Mendelian pattern and the fact that tumor cells exhibit characteristic morphologies on the basis of which they may be identified. Not all chromosomal changes induced by mutagens or carcinogens are necessarily irreversible. If the initial damage is small and localized, correction through the action of DNA-repairing enzymes is often still possible. Where repair is impossible and viable mutant cell lines are generated, hyperplastic or metaplastic lesions may appear which differ only slightly from the normal cells in the surrounding tissue. Such cell populations may coexist in healthy tissue for extended periods. In organisms with functional immunologic surveillance, “spontaneous” regressions may occur. But if the natural defense mechanisms are weakened, i.e., in old age or after exposure to stress, “carcinoma in situ” or small, avascular, solid tumors eventually appear.
This review was prepared with support from grant CHE76-10890 from the National Science Foundation, the Selenium-Tellurium Development Association, and the University of California Cancer Research Coordinating Committee. Helpful discussions with the late Dr. Klaus Schwarz are gratefully acknowledged.
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Schrauzer, G.N. (1979). Trace Elements in Carcinogenesis. In: Draper, H.H. (eds) Advances in Nutritional Research. Advances in Nutritional Research, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-9931-5_10
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