PREVENTION AND EARLY DETECTION OF CANCER - Otis W. Brawley, Barnett S. Kramer

INTRODUCTION

Cancer prevention and control is a burgeoning field because of advances in understanding the biology of carcinogenesis. The field has expanded beyond the identification and avoidance of carcinogens to include studies of specific interventions to lower cancer risk, as well as screening for early detection of cancer.

Central to cancer prevention and control is the concept that carcinogenesis is not an event but a process, a series of discrete cellular changes that result in progressively more autonomous cellular processes. Primary prevention concerns the identification and manipulation of the genetic, biologic, and environmental factors in the causal pathway. Smoking cessation, diet modification, and chemoprevention are primary prevention activities. Secondary prevention concerns the identification of asymptomatic neoplastic lesions combined with effective therapy. Screening is a form of secondary prevention.

EDUCATION AND HEALTHFUL HABITS

Public education on the avoidance of identified risk factors for cancer and encouraging healthy habits were among early efforts in cancer prevention and control. Many educational messages have come to the public through commercials in the print and electronic media and through school health courses. The physician is a potentially powerful messenger in this education campaign about the hazards of smoking, the benefits of a healthful diet and exercise, use of proven screening methods, and sun avoidance.

Smoking Cessation  Tobacco use through cigarettes and other means is the most avoidable risk factor for cardiovascular disease and cancer. The degree of smoke exposure, meaning the number of cigarettes smoked per day as well as the level of inhalation of cigarette smoke, is correlated with risk of lung cancer mortality. Light and low-tar cigarettes are not safer because smokers tend to inhale them more frequently and deeply. Those who stop smoking have a lower lung cancer mortality rate than those who continue smoking, despite the fact that some carcinogen-induced genetic mutations persist for years. In addition to lung cancer, cigarette smoking is a causative agent in cancers of the larynx, oropharynx, esophagus, bladder, and pancreas.

Smoking cessation and avoidance have the potential to save and extend more lives than any other public health activity. A smoker has a one in three lifetime risk of dying prematurely of a smoking-related cancer or cardiovascular or pulmonary disease. Indeed, more human lives are lost due to cardiovascular disease caused by smoking than from smoking-related cancer. The risk of tobacco smoke is not necessarily limited to the smoker. Epidemiologic studies suggest that environmental tobacco smoke may cause lung cancer and other pulmonary diseases in nonsmokers.

Nonsmoking persons should be encouraged not to start smoking, and persons who smoke should be encouraged to stop. Tobacco prevention is a pediatric issue. Over 80% of American smokers begin smoking before the age of 18. Nearly 20% of Americans aged 12 to 18 have smoked a cigarette in the past month. Counseling of adolescents and young adults is critical to prevent smoking. A physician's simple advice to not start smoking or to quit smoking can be of benefit. Physicians should query patients on tobacco use on every office visit, record the answer with the vital signs, and ask smokers if they would like assistance in quitting.

Current approaches to smoking cessation recognize that smoking is an addiction (Chap. 375). The smoker who is quitting goes through a process with identifiable stages that include contemplation of quitting, an action phase in which the smoker quits, and a maintenance phase. Smokers who quit completely are more likely to be successful than those who gradually reduce the number of cigarettes smoked or change to lower tar or nicotine cigarettes. More than 90% of the Americans who have successfully quit smoking did so on their own without participation in an organized cessation program, but cessation programs are helpful for some smokers. The Community Intervention Trial for Smoking Cessation (COMMIT) was a community-based 4-year program. COMMIT demonstrated that light smokers (<25 cigarettes per day) can benefit from simple cessation messages and cessation programs. The quit rate (fraction of the subjects followed who achieved and maintained cessation at the end of the trial) was 30.6% in the intervention communities and 27.5% in the control communities. This finding is statistically significant, but modest. The control communities enjoyed a substantial decrease in smoking through study participation. The COMMIT interventions were not successful for heavy smokers (>25 cigarettes per day). Heavy smokers need an intensive, broad-based cessation program that includes counseling, behavioral strategies, and pharmacologic adjuncts such as nicotine replacement and bupropion.

Cigar smoking has increased in the past 10 years, especially in younger adults. The health risks of cigars are similar to those of cigarettes. Smoking two cigars per day doubles the risk for oral and esophageal cancer; three to four cigars per day increases the risk of oral cancer eight-fold and esophageal cancer four-fold. The risks of occasional cigar smoking are unknown.

Smokeless tobacco is the fastest growing part of the tobacco industry and represents a significant health risk. Chewing tobacco is a carcinogen linked to dental caries, gingivitis, oral leukoplakia, and oral cancer. The systemic effects of smokeless tobacco may increase risks for other cancers.

Diet Modification  Dietary modification may have significant potential for lowering cancer risk in western culture. Studies of international dietary patterns and animal studies suggest that diets high in fat increase the risk for cancers of the breast, colon, prostate, and endometrium. These cancers have their highest incidence and mortalities in western countries, where fat comprises an average of 40 to 45% of the total calories consumed. In populations at low risk for these cancers, fat accounts for <20% of calories.

Despite correlations, dietary fat has not been proven to cause cancer. Case-control and cohort epidemiologic studies give conflicting results. In addition, diet is a highly complex exposure to many nutrients and chemicals. Low-fat diets may render some protection through anticarcinogens found in vegetables, fruits, legumes, nuts, and grains. Protective substances found in these foods include phenols, sulfur-containing compounds, flavones, and fiber.

In observational studies, dietary fiber appears protective against colonic polyps and invasive cancer of the colon. The mechanisms involved are complex and speculative. They involve binding of oxidized bile acids and generation of soluble fiber products, such as butyrate, that may have differentiating properties. Transit time is not greatly affected. High-fiber diets may also protect against breast and prostate cancer by absorbing and inactivating dietary estrogenic and androgenic cancer promoters. Protective effects of fiber have not been proved in a prospective clinical trial.

The Polyp Prevention Trial randomly assigned 2000 elderly persons to a low-fat, high-fiber diet versus routine diet for 4 years. No differences were noted in polyp formation.

The U.S. National Institutes of Health Women's Health Initiative, launched in 1994, is a long-term clinical trial enrolling more than 100,000 women aged 45 to 69. It studies the potential cancer-preventing effects of a low-fat diet and vitamin supplementation. Results are not yet available. Scientific evidence does not currently establish the anticarcinogenic value of vitamin, mineral, or nutritional supplements in amounts greater than that provided by a good diet. However, consuming at least five servings of fruits and vegetables a day decreases dietary fat and increases fiber; such a diet may lower the risk of cardiovascular disease.

Sun Avoidance  Nonmelanoma skin cancers (basal cell and squamous cell) are induced by cumulative exposure to ultraviolet radiation. Intermittent acute sun exposure and sun damage have been linked to melanoma. Sunburns, especially in childhood and adolescence, are associated with an increased risk of melanoma in adulthood. Reduction of sun exposure through use of protective clothing and changes in the pattern of outdoor activities can reduce skin cancer risk. Sunscreens decrease the risk of actinic keratoses, the precursor to squamous cell skin cancer, but melanoma risk may be increased. Sunscreens prevent burning and may encourage more prolonged exposure to the sun; yet they may not filter out wavelengths of energy that cause melanoma.

Educational interventions to help people assess their risk of developing skin cancer accurately have some impact. Self-examination for skin pigment characteristics associated with melanoma, such as freckling, may be useful in identifying people at high risk. People who recognize themselves as being at risk tend to be more compliant with sun-avoidance recommendations. Possible risk factors for melanoma include a propensity to sunburn, a large number of benign melanocytic nevi, and atypical nevi.