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Chemical and Physical Carcinogenesis: Advances and Perspectives for the 1990S1 [CANCER RESEARCH (SUPPL.) 51, 5023s-5044s, September 15. 1991] Chemical and Physical Carcinogenesis: Advances and Perspectives for the 1990s1 Curtis C. Harris2 Laboratory of Human Carcinogenesis, National Cancer Institute, N1H, Bethesda, Maryland 20892 Abstract the initiated cells with both an altered responsiveness to their microenvironment and moreover exerts a selective clonal ex Carcinogenesis is a multistage process driven by carcinogen-induced pansion advantage when compared to the surrounding normal genetic and epigenetic damage in susceptible cells that gain a selective cells (26-28). The initiated cells may have decreased respon growth advantage and undergo clonal expansion as the result of activation siveness to the inter- and intracellular signals that maintain of protooncogenes and/or inactivation of tumor suppressor genes. There fore, the mutational spectra of chemical and physical carcinogens in these normal tissue architecture and regulate the homeostatic growth critical genes are of interest to define endogenous and exogenous muta and maturation of cells. For example, initiated cells may be less tional mechanisms. The p53 tumor suppressor gene is ideally suited for responsive to negative growth factors, inducers of terminal cell analysis of the mutational spectrum. Such an analysis has revealed differentiation and/or programmed cell death (4, 26, 29-35). evidence for both exogenous and endogenous molecular mechanisms of Perturbation of the normal microenvironment by (a) physical Carcinogenesis. For example, an informative p53 mutational spectrum of means, e.g., wounding of the mouse skin or partial hepatectomy frequent G—»Ttransversions in codon 249 is found in hepatocellular carcinomas from either Qidong, People's Republic of China, or southern in rodents, (b) chemical agents, e.g., exposure of the mouse skin to certain phorbol esters or exposure of the rat liver to Africa. This observation links exposure to aflatoxin B,, a known cancer risk factor in these geographic regions, with a specific mutation in a phénobarbital,(c) the inflammatory process, or (d) microbial cancer-related gene. Other studies indicate that abnormalities in genes agents, e.g., influenza virus enhancement of rodent lung carci- controlling the cell cycle may cause genomic instability and increase the nogenesis or hepatitis viruses in human liver Carcinogenesis, probability of neoplastic transformation. Finally, mechanistic understand may also foster such selective clonal expansion of the initiated ing of Carcinogenesis is leading to improved cancer risk assessment and cells (4, 17, 36, 37). to the identification of individuals at high cancer risk. Tumor promotion results in proliferation and/or survival of the initiated cells to a greater extent than normal cells and Introduction enhances the probability of additional genetic damage including endogenous mutations accumulating in the expanding popula Carcinogenesis is a mature multidisciplinary field of cancer tion of these cells. The probability of a subpopulation of initi research that has a rich history of scientific accomplishments ated cells converting to malignancy can be substantially in achieved by epidemiológica! observations (1-3); development creased by their further exposure to DNA-damaging agents and exploitation of both animal models relevant to human (38-40) that may activate protooncogenes (41) and/or inacti cancer (4) and in vitro cell and tissue models including the use vate tumor suppressor genes. Malignant cells continue to ex of human tissues (5, 6); and most recently, advances in molec hibit progressive phenotypic changes during tumor progression ular genetics (7-II).3 Examples of conceptual advances and (42) and may exhibit intrinsic genomic instability that is man seminal observations in the areas of chemical and physical ifested by the abnormal number and structure of chromosomes, Carcinogenesis are listed in Table 1; advances in viral Carcino gene amplification, and altered gene expression (43-45). genesis are reviewed by Howley in this issue (12). This classical view of two stage Carcinogenesis involving a Since the research accomplishments of Carcinogenesis have mutation, tumor initiation, and an epigenetic change, tumor been extensively reviewed (13-25), this commentary will focus promotion, has been conceptually important but is also consid on selected topics that are especially relevant to current under ered to be simplistic in that the number of independent genetic standing of human Carcinogenesis and, in particular, to the and epigenetic events may be 6 or more in certain types of molecular epidemiology of human cancer, an emerging field in cancer (46-48). Furthermore, chemical carcinogens may: (a) cancer research. not be considered mutagens, termed nongenotoxic carcinogens (49); (b) have both genetic and epigenetic effects such as the Multistage Carcinogenesis ability to induce mutations and the property of decreasing DNA methylation, respectively (50) or increase cellular proliferation; Carcinogenesis is a multistage process driven by carcinogen- and (c) have a linear or non-linear dose-response relationship induced genetic and epigenetic damage in susceptible cells that with respect to tumor formation (51, 52). These and other gain a selective growth advantage and undergo clonal expansion observations have generated an active debate concerning both as the result of activation of protooncogenes and/or inactivation the contribution of endogenous mutagenic mechanisms, e.g., of tumor suppressor genes. The traditional view of carcinogen- oxy-radical DNA damage, DNA depurination, DNA polymer- esis (Fig. 1) is derived primarily from studies of animal models. ase infidelity, and deamination of 5-methylcytosine, versus ex The first stage of the carcinogenic process, tumor initiation, ogenous environmental mutagens and the value of animal bioas- involves exposure of normal cells to chemical, physical, or says to identify carcinogens and to aid in human cancer risk microbial carcinogens that cause a genetic change(s) providing assessment (53-63). This debate is not merely an academic one 1Presented at the Symposium "Discoveries and Opportunities in Cancer in that societal and regulatory decisions critical to public health Research: A Celebration of the 50th Anniversary of the Journal Cancer Research." are at issue. May 15, 1991, during the 82nd Annual Meeting of the American Association for Cancer Research, Houston, TX. 2To whom requests for reprints should be addressed, at Laboratory of Human Carcinogen Metabolism and DNA Damage Carcinogenesis, National Cancer Institute, N1H, Building 37, Room 2C05, Be thesda, MD 20892. 3 Due to space limitations and the breadth of this topic, comprehensive reviews Many chemical carcinogens require metabolic activation gen will be frequently cited and are the source of additional citations. erally to high energy electrophiles to exert their carcinogenic 5023s Downloaded from cancerres.aacrjournals.org on September 28, 2021. © 1991 American Association for Cancer Research. CARCINOGENESIS Table 1 Examples of advances in chemical and physical carcinogenesis" A. Cancer etiology I. Life-style factors (tobacco snuff or smoke) can cause human cancer. Hill. 1759(329) Soemmerring, 1795 (330) Doll and Hill. 1950(331) Wynder and Graham, 1950(332) 2. Occupational agents and factors can cause human cancer. a. Nun (childlessness) Ramazzini. 1713(333) b. Coal soot Pott, 1775(334) c. Sunlight Thiersch, 1875(335) d. Aromatic amines Rehn. 1895(337) e. Benzene DeLore and Borgman, 1928 (340) f. Ionizing irradiation Harting and Hesse, 1879 (336) Trieben, 1902 (338) Clune!, 1910(339) Martland and Humphries, 1929 (341) g. Asbestos Ministry of Labour and National Serv ice, 1949(342) Wagner et al., 1960(343) 3. Mixtures of chemicals (coal tar) can cause cancer in experimental animals. Yamagiwa and Ichikawa. 1918 (344) 4. Specific chemicals, e.g., dibenzanthracene or 2-naphthylamine, are carcinogens in experi Kennaway and Hieger, 1930 (345) mental animals. Hueper et al.. 1938(346) 5. Solid "inert" substances such as plastic can cause cancer when implanted s.c. in experimen Turner. 1941 (347) tal animals. 6. Naturally occurring compounds isolated from plants, e.g., croton oil, or marine organisms, Berenblum, 1941 (348) e.g.. teleocidin B and okadaic acid, have cocarcinogenic and/or tumor-promoting activities in Fujiki et al.. 1979(349) experimental animals. 7. Naturally occurring chemicals such as alkaloids from plants, ¡-.K--brackenfern (Pleritlium Cook el al., 1950(355) aquilinum). cycad. and Senecio, and fungal toxins, e.g.. aflatoxin B,. can be carcinogens in Schoentalf/a/.. 1954(356) experimental animals. Laquer, 1964(357) Evans and Mason, 1965 (358) Carnaghan, 1965(359) Wogan, 1966(360) Wogan and Newberne. 1967 (361) 8. yV-Nitrosamines can be carcinogenic in laboratory animals. Magee and Barnes. 1956 (362) 9. Cooking of red meat, fish, or specific amino acids can generate polynuclear aromatic hydro Kuratsume, 1956(363) carbons and, in some cases, heterocyclic amines that are carcinogenic in animal models. Lijinsky and Shubik, 1964 (364) Sugimura et al.. 1977(365) Kasai el al.. 1980(366) 10. Tobacco smoking and alcoholic beverages are human cancer risk factors and have multiplic Wynder el al.. 1957(367) ative effects. Keller. 1967(368) Rothman and Keller, 1972 (369) 11. Exposure of the human fetus to ionizing radiation increases risk of leukemia. Stewart étal.,1958(370) 12. Tobacco smoking and occupational exposure to asbestos increases
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