Prevention Strategies

Numerous investigators are taking advantage of our current knowledge of the mechanisms of carcinogenesis in human epithelial tissues to develop strategies for disrupting this process and thereby preventing cancer. As discussed earlier in this chapter, carcinogenesis proceeds by a multistep process, in which normal epithelial tissues acquire aberrant growth properties. These neoplastic cells progress to become invasive cancer. Historically, cancer therapy has addressed only the last phase of this process. Prevention strategies are now focusing on pre-invasive, yet neoplastic lesions.

Prevention strategies generally influence one or more of five processes in carcinogenesis (99). One strategy has been to inhibit carcinogen-induced initiation events, which lead to DNA damage. An important caveat to this strategy is that the intervention must be present at the time of carcinogen exposure to be effective. Once irreversible DNA damage has occurred, this type of strategy is ineffective in preventing cancer development.

Another strategy has been to inhibit initiated cell proliferation associated with the promotion stage of carcinogenesis. An advantage to this type of strategy is that interventions affecting promotion are effective after initiating events have occurred. Because humans are exposed to carcinogenicagents (e.g., chem icals in tobacco smoke, automobile exhaust) throughout their lifetimes, cancer preventive agents that work after initiating events have occurred are desirable. Two strategies of decreasing cell proliferation are induction of apoptosis, or cell death, and differentiation, which may or may not be associated with apo-ptosis. Induction of either differentiation or apoptosis will stabilize or decrease, respectively, overall cell number in a tissue.

A final strategy for preventing cancer is to inhibit development of the invasive phenotype in benign, or non-invasive, precancers that occur during the process of epithelial carcino-genesis.

Investigators are beginning to address the possibility that the efficacy of cancer prevention strategies may depend on both genetic and environmental risk factors affecting specific individuals. Mutationsldeletion of the APC tumor suppressor gene, discussed earlier, causes intestinal tumor formation in both rodents and humans. Increasing levels of dietary fat increases intestinal tumor number in rodent models (100). However, mice with a defective APC gene develop tumors even on low-fat diets. Thus, dietary modifications may reduce carcinogenesis in individuals without, but may be ineffective in individuals with, certain genetic risk factors for specific cancers. Recently, several large randomized studies conducted in the United States have failed to detect any protective effect of dietary fiber increase or dietary fat decrease on colon polyp recurrence (101).

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