© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 3, 215-225,
February 3, 1999
© 1999 Oxford University Press
REVIEW |
Mechanism-Based Cancer Prevention Approaches: Targets, Examples, and the Use of Transgenic Mice
Affiliations of authors: S. D. Hursting, Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, and Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville; S. M. Fischer, J. DiGiovanni, Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville; T. J. Slaga, Center for Cancer Causation and Prevention, The AMC Cancer Research Center, Denver. CO; J. M. Phang, Laboratory of Nutritional and Molecular Regulation, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD.
Correspondence to: Stephen D. Hursting, Ph.D., M.P.H.,Department of Epidemiology, Box 189, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030 (e-mail: shursting{at}request.mdacc.tmc.edu).
Humans are exposed to a wide variety of carcinogenic insults, including endogenous and man-made chemicals, radiation, physical agents, and viruses. The ultimate goal of carcinogenesis research is to elucidate the processes involved in the induction of human cancer so that interventions may be developed to prevent the disease, either in the general population or in susceptible subpopulations. Progress to date in the carcinogenesis field, particularly regarding the mechanisms of chemically induced cancer, has revealed several points along the carcinogenesis pathway that may be amenable to mechanism-based prevention strategies. The purpose of this review is to examine the basic mechanisms and stages of chemical carcinogenesis, with an emphasis on ways in which preventive interventions can modify those processes. Possible ways of interfering with tumor initiation events include the following: i) modifying carcinogen activation by inhibiting enzymes responsible for that activation or by direct scavenging of DNA-reactive electrophiles and free radicals; ii) enhancing carcinogen detoxification processes by altering the activity of the detoxifying enzymes; and iii) modulating certain DNA repair processes. Possible ways of blocking the processes involved in the promotion and progression stages of carcinogenesis include the following: i) scavenging of reactive oxygen species; ii) altering the expression of genes involved in cell signaling, particularly those regulating cell proliferation, apoptosis, and differentiation; and iii) decreasing inflammation. In addition, the utility for mechanism-based cancer prevention research of new animal models that are based on the overexpression or inactivation of specific cancer-related genes is examined.
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