INITIATION-PROMOTION MODEL FOR CHEMICAL CARCINOGENESIS in VS .NET

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INITIATION-PROMOTION MODEL FOR CHEMICAL CARCINOGENESIS
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Precarcinogen Direct Acting Carcinogen Proximate Carcinogen Ultimate Carcinogen Spontaneous Decomposition Noncritical Binding Apoptosis DNA Damage/Covalent Interaction with DNA (Oncogenes/Tumor Suppressor Genes/Apoptosis-Related Genes) Error prone repair or no repair followed Repair by cell replication Normal Cell Initiated Cell (cell can remain dormant) Promotion (clonal expansion: epigenetic process) Benign Tumor Progression (additional genetic events) Malignant Tumor Inactive Metabolites
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Figure 12.10 General aspects of chemically induced carcinogenesis.
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can be repaired and produce a normal cell. If there is error in the repair of the DNA or the DNA adduct is not repaired before the cell replicates, an error in the newly synthesized DNA could occur, and if so, a mutation would occur in the DNA of the daughter cell. If this change has occurred in a critical gene, for example, in a protooncogene or tumor suppressor gene, it would represent an important mutagenic event(s) in carcinogenesis. The mutationally altered cell or initiated cell has an altered genotype and may remain dormant (not undergo clonal expansion) for the lifetime of the animal. However, additional mutations or hits in critical genes followed by clonal expansion could lead to tumor development as described earlier in this chapter. In addition to this mechanism, chemical carcinogenesis in experimental models can be divided into at least three stages: termed initiation, promotion, and progression (Figure 12.10); this model is thus often referred to as the initiation/promotion model of chemical carcinogenesis. As mentioned above, the initiated cell may remain dormant (not undergo clonal expansion) for the lifetime of the animal. However, if the animal is repeatedly exposed to a tumor promoter, it will provide a selective growth advantage to the initiated cell, which will clonally expand and eventually produce a benign tumor. This process is termed tumor promotion and is an epigenetic process favoring the growth of cells with an altered genotype. The development of a malignant tumor from a benign tumor encompasses a third step, termed progression and involves additional genetic changes.
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12.5 INITIATION-PROMOTION MODEL FOR CHEMICAL CARCINOGENESIS
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Experimentally, the initiation-promotion process has been demonstrated in several organs/tissues including skin, liver, lung, colon, mammary gland, prostate, and bladder
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CHEMICAL CARCINOGENESIS
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X No tumors X X PPPPPPPX No tumors PPPPPPP No tumors X P P P P P P P P No tumors Time PPPPPPP Tumors PPPPPPP Tumors
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Figure 12.11 Initiation/promotion model. X = application of initiator, P = application of promoter.
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as well as in variety of cells in culture. While tumor promoters have different mechanisms of action and many are organ speci c, all have common operational features (Figure 12.11). These features include (1) following a subthreshold dose of initiating carcinogen, chronic treatment with a tumor promoter will produce many tumors; (2) initiation at a subthreshold dose alone will produce very few if any tumors; (3) chronic treatment with a tumor promoter in the absence of initiation will produce very few if any tumors; (4) the order of treatment is critical as it must be rst initiated and then promoted; (5) initiation produces an irreversible change; and (6) promotion is reversible in the early stages, for example, if an equal number of promoting doses are administered but the doses are spaced further apart in time, tumors would not develop or would be greatly diminished in number. Many tumor promoters are organ speci c. For example, 12-O-tetradecanoylphorbol-13-acetate (TPA) also known as phorbol 12myristate 13-acetate (PMA) belongs to a family of compounds known as phorbol esters. Phorbol esters are isolated from croton oil (derived from the seeds of the croton plant) and are almost exclusively active in skin. Phenobarbital, DDT, chlordane, TCDD and peroxisome proliferators Wy 24,643, clo brate, and nafenopin are hepatic tumor promoters. TCDD is also a promoter in lung and skin. Some bile acids are colonic tumor promoters, while various estrogens are tumor promoters in the mammary gland and liver. There are multiple mechanisms of tumor promotion, and this may explain the organ speci c nature of the many promoters. Under conditions in which the chemical produces tumors without tumor promoter treatment, the chemical agent is often referred to as a complete carcinogen. It is generally accepted that tumor promoters allow for the clonal expansion of initiated cells by interfering with signal transduction pathways that are involved in the regulation of cell growth, differentiation, and/or apoptosis (Table 12.6). While the precise mechanisms of tumor promotion are not completely understood at the molecular/biochemical level, current research is providing new and promising mechanistic insights into how tumor promoters allow for the selective growth of initiated cells.
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