Much of the promise for cancer prevention comes from observational epidemiologic studies that show associations between modifiable lifestyle factors or environmental exposures and specific cancers. Evidence is now emerging from randomized controlled trials designed to test whether interventions suggested by the epidemiologic studies, as well as leads based on laboratory research, result in reduced cancer incidence and mortality.
The most consistent finding, over decades of research is the strong association between tobacco use and cancers of many sites. Hundreds of epidemiologic studies have confirmed this association. Further support comes from the fact that lung cancer death rates in the United States have mirrored smoking patterns with increases in smoking followed by dramatic increases in lung cancer death rates, and more recently decreases in smoking followed by decreases in lung cancer death rates in men.
Infections may also be associated with cancer development. Human papillomavirus (HPV) infection is a necessary event for subsequent cervix cancer, and vaccine-conferred immunity results in a marked decrease in precancerous lesions. Likewise, Epstein-Barr virus has been associated with Burkitt lymphoma and Helicobacter pylori with gastric cancer, although specific anti-infective interventions have not yet proven effective in preventing these cancers. Additional examples of modifiable cancer risk factors include alcohol consumption (associated with increased risk of oral, esophageal, breast, and other cancers), physical inactivity (associated with increased risk of colon, breast, and possibly other cancers), and obesity (associated with colon, breast, endometrial, and possibly other cancers). Observational evidence shows associations between alcohol consumption, physical inactivity, and obesity and increased incidence of certain cancers. More research is needed to determine whether these associations are causal and whether avoiding these behaviors would actually reduce cancer incidence. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexual and reproductive practices, the use of exogenous estrogens, exposure to ionizing radiation and ultraviolet radiation, certain occupational and chemical exposures, and infectious agents.
Food and nutrient intake have been examined in relation to many types of cancer. As a general rule, epidemiological studies have suggested associations between diet and cancer development, but prospective observational or interventional studies have not provided strong support. For example, case-control epidemiological studies suggest an association between high fruit and vegetable consumption and reduced risk of various cancers, but prospective cohort studies have not observed such strong protective associations. On the basis of population-based epidemiologic data, high-fiber diets were recommended to prevent colon neoplasms, but a randomized controlled trial of supplemental wheat bran fiber did not reduce the risk of subsequent adenomatous polyps in individuals with previously resected polyps. Ecologic, cohort, and case-control studies found an association between fat and red meat intake and colon cancer risk, but a randomized controlled trial of a low-fat diet in postmenopausal women showed no reduction in colon cancer. The low-fat diet did not affect all cancer mortality, overall mortality, or cardiovascular disease. Multivitamin and mineral supplements have been advocated for cancer prevention, but the evidence is insufficient to support their use. For example, beta carotene was thought to prevent or reverse smoking-related changes leading to lung cancer, but two prospective placebo-controlled trials found that smokers and former smokers had increased lung cancer incidence and mortality. A large randomized trial is currently under way to investigate whether men taking daily selenium or vitamin E or both experience a reduced incidence of prostate cancer in comparison with men taking placebo pills. Chemoprevention trials have had some positive results. Daily use of selective estrogen receptor modulators (tamoxifen or raloxifene) for up to 5 years reduces the incidence of breast cancer in high-risk women by about 50%. Finasteride (an alpha-reductase inhibitor) lowers the incidence of prostate cancer, although the occurrence of more high-grade cancers in treated men is poorly understood. Other chemoprevention candidates include COX-2 inhibitors (which inhibit the cyclooxygenase enzymes involved in the synthesis of proinflammatory prostaglandins) to prevent colon and breast cancer, although the possibility of increased cardiovascular events may preclude their usefulness. Statins have been proposed as cancer-prevention agents, but on review many retrospective studies show that they probably neither increase nor decrease cancer risk.
Considerable research effort is now devoted to potential venues for gene therapy for individuals with genetic mutations or polymorphisms that put them at high risk of cancer. Meanwhile, genetic testing for high-risk individuals with enhanced surveillance or prophylactic surgery for those who test positive is already available for certain types of cancer including breast and colon cancers.