According to the American Cancer Society (ACS), more than a half million Americans will die of cancer in 2004-that is more than 1,500 people a day. One of every four deaths in America is from cancer. About 1.4 million new cases of cancer will be diagnosed in 2004. This estimate does not include diagnoses of in situ (preinvasive) cancer (except for urinary bladder cancer) or the approximately 1 million cases of nonmelanoma skin cancer that will be diagnosed this year.
The National Cancer Institute (NCI) estimates that about 9.6 million Americans with a history of cancer were alive in January 2000. Although some of these individuals were considered to be cured or cancer free, others continued to live with the disease and may have been receiving treatment.
Effective strategies exist for reducing the number of both new cases of cancer and deaths caused by cancer. These include decreasing theprevalence of behavioral and environmental factors that increase people's cancer risk and ensuring that evidence-based screening tests and treatment services are available and accessible. Resources that can be devoted to such strategies are limited, and must be allocated wisely. Wise resource allocation, in turn, depends partly on the availability of complete, timely, and high-quality cancer data.
Much of the promise for cancer prevention comes from observational epidemiologic studies that show associations between modifiable life style 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 andmortality.
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.
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 being overweight(associated with colon, breast, endometrial, and possibly other cancers). Based on epidemiologic evidence, it is now thought that avoiding excessive alcohol consumption, being physically active, and maintaining recommended body weight, may all contribute to reductions in risk of certain cancers; however, compared with tobacco exposure, the magnitude of effect is modest or small and the strength of evidence is often weaker. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexual and reproductive practices, the use ofexogenous 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. Fruit and vegetable consumption have generally been found in epidemiologic studies to be associated with reduced risk for a number of different cancers. Contrary to expectation, randomized trials found no benefit of beta-carotene supplementation in reducing lung cancer incidence and mortality; risk of lung cancer was statistically significantly increased in smokers in the beta-carotene arms of 2 of the trials. Similarly, randomized controlled trials have found no reduction in risk of subsequent adenomatous polyps of the colon in individuals who have had polyps previously resected taking dietary fiber supplements compared with those receiving much lower amounts of supplemental wheat bran fiber. On the other hand, there is evidence from at least 1 randomized controlled trial that calciumsupplementation does modestly reduce risk of adenoma recurrence. Consumption of red meat and inadequate folic acid intake have also been associated with increased risk of colon cancer. A large randomized trial is currently underway to investigate whether men taking daily selenium orvitamin E or both experience a reduced incidence of prostate cancer in comparison to men taking placebo pills. A meta-analysis of 19 randomized trials suggests that vitamin E supplements do not decrease the risk of all-cause mortality.
Daily use of tamoxifen, a selective estrogen receptor modulator, for up to 5 years, has been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%. Cis-retinoic acid also has been shown to reduce risk of second primary tumors among patients with primary cancers of the head and neck. Finasteride, an alpha-reductase inhibitor, has been shown to lower the risk of prostate cancer. Other examples of drugs that show promise for chemoprevention include COX-2 inhibitors(which inhibit the cyclooxygenase enzymes involved in the synthesis of proinflammatory prostaglandins).
Considerable research effort is now devoted to the development of vaccines to prevent infection by oncogenic agents, and 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.
Screening for colon cancer through fecal occult blood testing has been demonstrated to reduce both colon cancer incidence and mortality, presumably through the detection and removal of precancerous polyps. Similarly, cervical cytology testing (using the Pap smear) leads to the identification and excision of precancerous lesions. Over time, such testing has been followed by a dramatic reduction of cervical cancer incidence and mortality.
Sources: Centers for Disease Control and the National Cancer Institute
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