In many respects, cancer is a preventable disease. Estimates indicate that approximately one half of all cancer cases either arise from modifiable risk factors or can be detected as precursor lesions before the development of disease with metastatic potential. 
Prevention of cancer can take place on several different levels:
Although cancer has overtaken cardiovascular disease to become the leading cause of death in men and women younger than 85 years in the United States, and the number of cancer deaths continues to increase with the aging and growth of the population, age-standardized US death rates from cancer have been decreasing.  The US cancer death rate peaked at 215.1 per 100,000 population in 1991 and declined to 166.4 per 100,000 population in 2012. The overall incidence rate of cancer in women has remained stable since 1998, but in men it has declined by 3.1% per year since 2009. 
These declines have been attributed to risk reduction strategies, detection of early disease, and improvement in treatment strategies. This review addresses the first 2 of those factors, to summarize the evidence for prevention in oncology.
Assessment of an individual’s risk is a key step in cancer prevention; risk assessment programs have been developed at many cancer centers to identify people who are at high risk. Review of personal and family medical history, work history, and lifestyle can help identify cancer risk factors, which may be modifiable (eg, tobacco use, sun exposure) or nonmodifiable (eg, family history of cancer, sex, ethnicity, race, advancing age, hormone levels). Combinations of modifiable and nonmodifiable risk factors place some people at particularly high risk for cancer.
Models of cancer risk have been developed to permit calculation of an individual’s risk for a specific type of cancer. One of the best known of these is the Gail model, which predicts breast cancer risk on the basis of current age, race, age when menstruation began, age of first live birth, number of close relatives with breast cancer, number of breast biopsies, and the presence or absence of atypical hyperplasia on breast biopsies.  Like most cancer risk models, the Gail model has limitations: it does not include ovarian cancer history or breast cancer in second-degree relatives such as aunts, cousins, or grandparents. This model may also be less accurate in predicting risk in non-white women. Therefore, risk models should be selected based on each individual’s situation in order to calculate risk as accurately as possible.
Overall, approximately 10% of cancers occur because of hereditary predisposition, such as mutations in cancer susceptibility genes (eg, BHCA1 and BRCA2). Many of these mutations can be identified through analysis of a blood or tissue sample. Currently, genetic testing is recommended only for individuals who have a personal or family history that is suggestive of an inherited cancer syndrome.
A study by Reulen et al found that survivors of childhood cancer are at excess risk of developing primary neoplasms later in life, with the greatest risk for digestive and genitourinary neoplasms in survivors older than 40 years. 
Identification of the appropriate person for testing leads to more informative results for the entire family. In most cases, the person who has had the cancer that best fits the hereditary pattern should be chosen for testing. If a mutation is identified in this individual, others in the family who are at risk can then be tested for that specific mutation. Genetic analysis should always be preceded by careful genetic counseling, which continues after determination of gene mutation status. Identification of a genetic alteration may change recommendations for cancer screening, chemoprevention, and prophylactic surgery.
In addition to risk from genetic syndromes, it is estimated that approximately another 15-20% of cancers are familial, which may be due to low-penetrance genetic changes or the effects of shared environment and behaviors. The remainder of cancers in the general population are considered sporadic.
Modifiable risk factors for cancer include tobacco use, sun exposure, diet, exercise, obesity, alcohol use, hormone replacement therapy (HRT), environmental/occupational exposures, infectious exposures, and sexual activity.
Tobacco use accounts for almost one third of cancer deaths in the US.  Of these, lung cancer is the most common, but cancers of the blood, head and neck, esophagus, liver, pancreas, liver, stomach, cervix, kidney, colon, and bladder have also been linked to smoking.  Many chemicals are present in tobacco smoke, including at least 69 known carcinogens.  Smokeless tobacco—chewing tobacco and dipping snuff—contains at least 28 carcinogens. 
Smoking may also promote more aggressive forms of cancer: for example, tobacco use is associated with higher-grade and higher-stage prostate cancer.  Secondhand smoke, also known as environmental tobacco smoke, has been associated with both lung and sinus cancers in nonsmokers.  ln addition, considerable evidence indicates that smokeless tobacco and cigars also have deadly consequences, including lung, laryngeal, esophageal, and oral cancers. 
Carcinogenesis from tobacco use occurs through several mechanisms, including direct delivery of carcinogens to tissues, inflammation, and breakdown of physiologic barriers.  Cessation of tobacco use has been shown to reduce both cancer-related and all-cause mortality. Health benefits start soon after quitting and can be seen even in long-time users.  For former smokers who have been abstinent for 10 years, the risk of lung cancer is one half that of current smokers. This risk falls to as low as 10% for ex-smokers who have quit for 30 years or more. Moreover, the risk for cancers of the mouth, throat, and esophagus lessens significantly 5 years after quitting, and the risk of developing bladder or cervical cancers also decreases after just a few years of being nicotine free. 
Most individuals require several quit attempts before they are able to stop smoking. The addiction to tobacco use is both psychologic and biochemical. Medications are available to address the biochemical aspects, whereas counseling and other social support are recommended for treating the psychologic aspects.
Nicotine replacement therapy provides nicotine without the other components of tobacco and can be administered through a patch, nasal spray, chewing gum, lozenge, or inhaler. Clinical trials have demonstrated that the use of nicotine replacement doubles the rate of quitting tobacco use. 
The addition of bupropion (Zyban), an antidepressant medication, may increase the efficacy of nicotine replacement.  A meta-analysis has also shown that bupropion doubles the quit rate when used as monotherapy.  However, this medication should be avoided in individuals with a history of seizures or eating disorders.
The newest medication for smoking cessation is varenicline (Chantix),which was found to be superior to bupropion in 3 clinical trials. [18, 19, 20] Unblinded studies comparing varenicline and nicotine replacement suggested that the quit rates may be higher with varenicline. [21, 22] However, a randomized controlled trial that compared 12 weeks of treatment with nicotine patch only (n=241), varenicline only (including 1 pre-quit week; n=424), nicotine patch + nicotine lozenge (n=421) found no significant differences in carbon monoxide–confirmed rates of smoking abstinence at 26 weeks. 
Individuals with depression or other neuropsychiatric disorders should not take varenicline, as this medication may exacerbate their symptoms. Both varenicline and bupropion appear to be safe in pregnancy. 
A randomized controlled trial in 385 1 pack/day smokers found that treatment with bupropion plus varenicline did not appear to increase smoking abstinence rates above that seen with varenicline alone.  However, a prospective study concluded that a particular subset of smokers—males with a baseline Fagerstrom Test for Nicotine Dependence (FTND) score ≥ 6 and cigarette consumption ≥ 20/day—benefited substantially from combination therapy with varenicline plus bupropion: after 12 weeks of treatment, the abstinence rate the abstinence rate was 71.0% with combination therapy versus 43.8% with varenicline plus placebo. 
Of course, the ideal way to reduce tobacco-associated cancers is for people to not start using tobacco in the first place. Community programs for youth and public service announcements are 2 means of addressing this issue.
Nonmelanoma skin cancers comprise 40% of malignancies in the US. The incidence rates of melanoma, although much less common than nonmelanoma skin cancers, is increasing and this condition has a much higher propensity for metastasis and death.
Ultraviolet radiation is a well-established carcinogen for both melanoma and nonmelanoma skin cancers. However, the patterns of sunlight exposure associated with these cancers differ significantly. Squamous cell carcinoma tends to occur in those who have chronic sun exposure, often due to occupational exposure from working outdoors. [27, 28]
Episodes of intense ultraviolet exposure, particularly in children and others without a history of chronic sun exposure, is associated with melanoma incidence,  and a history of blistering sunburns more than doubles the risk of melanoma.  Basal cell carcinoma, although usually associated with chronic sun exposure, has also been linked to intermittent exposure in a significant proportion of cases.  In addition, the use of tanning beds has been associated with increased skin cancer incidence  ; in fact, the World Health Organization (WHO) has recommended against the use of these devices for individuals younger than age 18 years. 
Recent interest in vitamin D as a chemopreventive agent for several types of cancer has made sun avoidance a controversial topic, because this nutrient is most easily and effectively obtained from sun exposure. Several clinical trials with vitamin D are planned or under way, and this remains an area of active investigation in cancer prevention. However, at this time, most groups recommend limiting exposure to the sun during peak hours (between 10 AM and 4 PM); using protective clothing, including hats and sunglasses; and using sunscreens with a sun protection factor (SPF) of 30 or greater. Sunscreens should be broad-spectrum and contain agents that work against both ultraviolet (UV) A and UVB radiation (eg, oxybenzone, avobenzone, titanium dioxide, or zinc oxide).
Proper use of sunscreen is also critical: regardless of the SPF, all sunscreen should be applied approximately 30 minutes before sun exposure and then reapplied liberally at least every 1.5-2 hours or after swimming or perspiring heavily. A randomized clinical trial demonstrated statistically significant protection against squamous cell carcinoma with regular use of sunscreen; however, it should be noted that this protective effect did not extend to basal cell carcinoma and that the study was underpowered to assess effect on melanoma risk.  Several meta-analyses have assessed the effects of sunscreen use on melanoma risk and found no association. [35, 36, 37] Therefore, sun avoidance and clothing protection remain the mainstays of skin cancer prevention as well.
Multiple components of the diet have been studied, both singly and in combination, for their effects on cancer risk. However, study of diet has proven difficult. Epidemiologic studies may have limited reliability because of inaccurate recall and multiple confounding factors, whereas clinical trials are subject to noncompliance, inappropriate form of the nutrient, or an insufficient follow-up period. 
Total dietary fat appears to affect the incidence of prostate cancer but has not been consistently proven to affect rates of colon or breast cancer.  lt should be noted that fat intake is generally evaluated with adjustments for caloric intake and weight gain in order to isolate any effects of the fats themselves. Additional investigation of the effects of types of fat is ongoing. Individuals with high levels of consumption of red meat have been found to have an increased risk of colorectal cancer. [40, 41, 42, 43, 44]
Some dietary practices appear to reduce cancer risk. The link between fruit and vegetable intake and decreased overall cancer risk is weak [45, 46] ; however, pooled analyses suggest a 25% reduction in the incidence of distal (but not proximal) colon cancer in those who consumed more than 800 g of fruits and vegetables per day.  Studies focused on tomato products suggest a benefit for prostate cancer risk, possibly due to the lycopene content in these foods. 
Consumption of calcium has been associated with a decreased incidence of any cancer in women and a decreased incidence of colon cancers in both men and women.  Epidemiologic studies have found that increased fiber intake is associated with a decreased risk of colon cancers and adenomas; however, clinical trials of a high-fiber diet showed no effect on the rates of adenoma recurrence. [50, 51, 52, 53]
Overall, dietary recommendations from the American Cancer Society (ACS) include (1) eating a variety of healthful foods, with 5 or more servings of vegetables and fruits per day; (2) use of whole grains in preference to processed (refined) grains and sugars; and (3) limited consumption of red meats, especially processed meats and those high in fat. 
Estimates indicate that a sedentary lifestyle is responsible for approximately 5% of cancer deaths.  Higher levels of physical activity have been associated with decreases in the risks of colon and breast cancers, and possible decreased risks of endometrial, prostate, liver, pancreatic, stomach, and lung cancers have been described as well. [56, 57, 58, 59, 60, 61, 62] For colon and breast cancers, the benefit of physical activity has been demonstrated at multiple weight levels, which implies that the effect of the activity is independent of an effect of weight reduction. The mechanism of the protective effect remains uncertain but may be related to effects on immunity, hormone levels, or prostaglandins.
The frequency, duration, or intensity of exercise needed to prevent cancer has not been determined definitively. The American Cancer Society recommends that adults engage in moderate exercise for at least 30 minutes on 5 or more days per week. Increasing the length of exercise to 45 minutes or more may provide additional protection against breast and colon cancer. For children, the recommendation is to exercise for at least 60 minutes per day on at least 5 days per week. 
Epidemiologic studies have indicated that excess weight or obesity result in 14% of cancer deaths in men and 20% of cancer deaths in women.  The cancers associated with obesity are similar to those associated with decreased physical activity. Excess weight has been found to account for 10-40% of colorectal, endometrial, renal, esophageal, and postmenopausal breast cancers. 
Possible links have also been described for some hematologic malignancies and cancers of the prostate, liver, gallbladder, pancreas, stomach, ovary, and cervix, as well. Interventions such as bariatric surgery may reduce the risk of cancer deaths by as much as 60%. 
Long-term alcohol use has been associated with approximately 4% of incident cancer cases.  In a study of a large database of women, 1 alcoholic beverage per day increased overall cancer risk by 6%.  The increase in cancer incidence in this group involved increased risks of cancers of the head and neck, esophagus, rectum, liver, and breast. The Women’s Health Study also showed an increase in breast cancer risk associated with moderate alcohol consumption. 
The mechanism of carcinogenesis associated with alcohol use is not fully understood at this time but may involve inflammatory, epigenetic, hormonal, or metabolic effects. Several of the metabolites of ethanol have been identified as carcinogens.  The American Cancer Society recommends limiting alcohol use to 2 drinks per day for men and 1 drink per day for women (due to the slower metabolism of alcohol by women). A drink is 12 ounces (oz) of beer, 5 oz of wine, or 1.5 oz of 80-proof liquor.
Considerable epidemiologic evidence suggests that the duration of a woman’s exposure to endogenous estrogen affects breast cancer risk. Support for this hypothesis includes the increased risk of breast cancer for women with an earlier age of menarche, later age of menopause, nulliparity, and later age at first live birth, as well as higher serum estrogen concentrations. For women who take estrogen-only hormone replacement therapy, meta-analyses of epidemiologic studies indicate a mildly increased risk of breast cancer. [70, 71, 72, 73]
The primary clinical trial to investigate this question was the Women’s Health Initiative trial, in which estrogen-only hormone replacement therapy was not found to increase breast cancer risk when results were reported at a mean follow-up of 7.1 years.  However, combination therapy with estrogen-progestin hormone replacement did demonstrate a significantly increased risk, with a hazard ratio of 1.2.  This risk remained elevated for several years after discontinuation of combination therapy but then declined rapidly.  After the results of the Women’s Health Initiative study were made public, a subsequent decline in breast cancer incidence was noted in the US, which has been attributed, in part, to a decrease in the use of combination hormone replacement. 
Hormone replacement therapy has been shown to increase breast density, which, in turn, decreases the sensitivity of mammograms. [78, 79] In the Women’s Health Initiative study, postmenopausal women on combination progesterone/estrogen replacement had an average increase of 6% in mammographic density, whereas their counterparts taking placebo had an approximately 1% decrease over the same period. 
Geographic patterns of cancer incidence may provide insight into cancer etiology. Possible risk
factors include environmental exposures and occupational exposures from the air or water.
Workplace exposure to chemicals such as coal-tar–based products, benzene, cadmium, uranium, asbestos, or nickel can significantly increase cancer risk. For example, a significant proportion of bladder cancers may be due to chemical exposures in the aluminum, dye, paint, petroleum, rubber, and textile industries. Occupational exposures to radon and asbestos have been linked to lung cancer, and a small percentage of lung cancers are attributable to air pollution. Arsenic exposure has also been linked to increased incidence of nonmelanoma skin cancers. 
The International Agency for Research on Cancer (IARC) has conducted extensive evaluations of potential carcinogens based on data from epidemiologic and animal studies. They define a carcinogenic agent as one capable of increasing the incidence of malignant neoplasms, reducing their latency, or increasing their severity or multiplicity.  At this time, 108 agents are classified as group 1, or agents that are known to be carcinogenic to humans. Another 66 agents are classified as group 2A, or probable carcinogens in humans. Monographs detailing the evaluations of these agents can be accessed on the IARC website.
Approximately 17% of cancers occurring worldwide may be attributed to an infectious etiology.  The primary cancers with known associations with viral infections include:
Cervical and anogenital cancers (human papillomavirus [HPV])
Kaposi sarcoma (human herpes virus [HHV]-8)
Adult T-cell leukemia (human T-cell lymphotropic virus -1 [HTLV-I])
Infection with human immunodeficiency virus (HIV) also increases the risk of Kaposi sarcoma and non-Hodgkin lymphoma. In some instances, these cancers may be acquired immunodeficiency syndrome (AIDS) – defining malignancies.
Measures to prevent transmission of viral carcinogens include vaccination against carcinogenic types of HPV (see Vaccines and Medical Prevention), use of sterile needles in the healthcare and community (eg, tattoo and drug use) settings, and screening of potential blood donors. The estimated risk of hepatitis infection via blood transfusion is approximately 1 in 58,000 to 269,000 for HBV and 1 in 2 million for HCV. Risk of transmission of HTLV-1 by transfusion is 1 in 2 million, and that of HIV infection by transfusion is approximately 1 in 2 million. [86, 87, 88]
For individuals who are infected with a virus that has the potential to cause cancer, several interventions are possible. Treatment of HIV infection with highly active antiretroviral therapy (HAART) can prevent lymphomas associated with this virus.  Similarly, treatment of chronic HBV infection with interferon or nucleotide analogues to reduce the viral load also decreased the incidence of hepatocellular carcinoma.  Alcohol avoidance may also decrease the development of hepatoma in those with chronic hepatitis.
Bacterial infection with Helicobacter pylori is associated with risk of gastric cancer. Some data suggest that eradication of H pylori infection through regimens of antibiotics and proton pump blockers may be effective as primary prevention of gastric cancer. [91, 92, 93] This approach is currently being evaluated in a large-scale international clinical trial.
Because some viral carcinogens are transmitted via bodily fluids, increased numbers of sexual partners or sexual contact with infected partners can increase the risk of these cancers. Although most women are exposed to HPV in their lifetime, infection is usually transient. When this virus cannot be cleared by the body, cervical cancer may develop. For this reason, individuals who have multiple sexual partners or who have a compromised immune system are more susceptible to HPV infection.
Means of reducing sexual transmission of carcinogenic viruses include awareness of the sexual and medical history of partners and use of barrier methods such as a condom during sexual intercourse.
Screening for breast cancer can include different tests, of which clinical breast examination (CBE) and mammography are commonly used.
Studies have shown that breast self-examination (BSE) does not affect breast cancer diagnosis, mortality, or stage at diagnosis. [94, 95] In other studies, however, individuals who performed more thorough examinations did appear to derive a benefit. [96, 97] The US Preventive Services Task Force (USPSTF) recommends against teaching BSE.  However, many experts continue to include self-examination in their recommendations due to the low cost and the benefit of making the patient an active participant in her health.
American Cancer Society (ACS) guidelines advise that it is acceptable for women to choose not to do BSE or to do BSE regularly (monthly) or irregularly. Beginning in their early 20s, women should be told about the benefits and limitations of BSE. Whether a woman ever performs BSE, the importance of prompt reporting of any new breast symptoms to a health professional should be emphasized. Women who choose to do BSE should receive instruction and have their technique reviewed on the occasion of a periodic health examination. 
Clinical breast examination
When performed correctly by trained medical personnel in combination with mammography, clinical breast examination has greater sensitivity but a higher false-positive rate than mammography alone.  One study suggested, however, that the overall effect on the cost-benefit ratio could be considered detrimental, as 55 false-positive results were identified for every cancer detected by examination that was not detected on mammography. In practice, nonstandardized breast examinations have a sensitivity of about 36% but detect about 5% of cancers not visible on mammograms. 
Overall, in settings in which mammography is available, clinical breast examination may provide a slight improvement in breast cancer detection. Nevertheless, the ACS does not recommend clinical breast examination for breast cancer screening in average-risk women at any age.  However, clinical breast examination is a cost-effective measure in countries that do not have access to imaging resources. 
Since 1990, the mortality rate from breast cancer has been declining approximately 2% per year.  A study using several statistical models estimates that use of screening mammograms accounts for 28-65% of that reduction (median, 46%).  A meta-analysis of randomized controlled trials showed a significant 34% reduction in breast cancer mortality at 7 years in those who had mammographic screening.  A subsequent review indicated that the survival benefit from mammography was greater in women older than 50 years than in those between the ages of 40 and 49 years.  However, numerous other studies have demonstrated decreased mortality in women in their 40s as well. [106, 107, 108, 109] Despite this evidence of a mortality benefit, mammogram screening rates in the US decreased between 2000 and 2005. 
Types of mammograms in use include film mammograms and digital mammograms. Images from digital mammograms are electronically captured and stored, whereas those from film mammograms are provided via traditional radiographic films. Overall, cancer detection rates are similar regardless of which type of mammogram is used. [111, 112, 113, 114, 115] The exceptions to this rule are that digital mammography is more accurate in premenopausal women and in women with dense breasts. 
Most experts agree that screening mammography should be performed routinely in women between the ages of 50 and 69 years. The frequency of screening in this population has been a controversial issue, however, as has the use of screening in younger women. Guidelines vary in their recommendations on these topics, and place increasing emphasis on patient choice.
For women between the ages of 50 and 69 years, some guidelines recommend annual mammography, whereas others advocate biennial or annual examination; Canadian guidelines recommend mammography every 2 to 3 years (weak recommendation). [117, 118, 119] Data that directly address this question are sparse, but one observational study comparing annual and biennial screening showed no significant disadvantage from the biennial schedule in terms of detection rate or stage at time of diagnosis. 
For women age 40 to 49, the breast cancer incidence and the sensitivity of mammograms are both lower than they are in women aged 50-69 years. The ACS recommends that average-risk women start annual mammograms at age 45 and consider transitioning to biennial screening at age 55. 
The American College of Physicians (ACP) and the Advisory Committee on Cancer Prevention in the European Union advise discussion of screening with patients and shared decision-making. [121, 122] The American College of Obstetricians and Gynecologists (ACOG) recommends offering mammography at ages 40 to 49 and, if after counseling the patient desires it, initiating annual or biennial screening. 
Other groups, such as the Canadian Task Force on Preventive Health Care, recommend deferring mammography until the age of 50 years in the absence of family history or other risk factors.  The USPSTF recommends against routine mammography in women aged 40-49 years, instead advocating that physicians discuss the risks and benefits of biennial screening with women in this age group. 
Data are conflicting in this area: a significant decrease in breast cancer mortality was found on meta-analysis of those who started screening in their 40s  but not in a larger randomized clinical trial of annual mammography versus usual care.  A cost-effectiveness study has shown that mammograms cost $21,400 per year of life saved for women aged 50-69 years, whereas the cost was $105,000 per year of life saved for women in their 40s.  Although the cost for women in their 40s was 5-fold higher, both of these values fall within the accepted range for cost effectiveness.
Recommendations for when to stop mammography also vary. The USPSTF concluded that the current evidence is insufficient to assess the balance of benefits and harms of screening mammography in women aged 75 years or older.  ACOG guidelines recommend that whether to continue mammography after age 75 should involve shared decision-making that includes a discussion of the woman’s health status and longevity.  . The ACS recommends that women continue screening mammography as long as their overall health is good and they have a life expectancy of 10 years or longer. 
It has been suggested that bone mineral density (BMD) be incorporated into decision-making for breast screening for individuals in this 70-79 year age group, as those with higher bone density have an increased risk of breast cancer compared with those with low bone mineral density.  A general rule that has been suggested for this population is that screening continue for those who have a life expectancy of 10 years or greater.
The false-positive rate of mammography is approximately 11% in the US.  Risk factors for a false-positive result include younger age, previous breast biopsy, family history of breast cancer, current estrogen use, inconsistent screening, and lack of previous mammograms for comparison.  Women with a false-positive result on a mammogram will be called back for additional imaging and possible biopsy of a lesion that is ultimately found to be benign.
Overdiagnosis, or screen detection of cancers that would normally not cause clinical morbidity or affect mortality, remains an issue with mammography. Estimates of overdiagnosis range from 1 in 3 to 1 in 6 cancers detected by screening mammogram. [128, 129]
Some women express concern regarding the radiation associated with regular mammographic screening. Direct data regarding the risk associated with this level of radiation exposure are lacking, but a study of a risk model comparing the risk of radiation and the mortality benefit of mammographic detection concluded that the net effect of mammograms was positive for women older than age 40 years. 
However, it is important to note that women with BRCA mutations may be more susceptible to the effects of radiation to the breast. Studies of BRCA carriers showed that those with exposure to chest x-rays were 54% more likely to develop breast cancer; this risk increased with multiple x-rays or x-rays done at an early age.  In contrast, a study of mammograms in another BRCA population did not find an increased risk of breast cancer in a multivariate model. 
In the US, breast ultrasonography is not usually performed as a screening study. Investigations into the combination of ultrasonography and mammography for screening have shown increased sensitivity but decreased specificity with the addition of ultrasonography. [133, 134, 135] At present, although ultrasonography remains a tool for diagnosis, it is not a tool for screening of the breast.
Breast magnetic resonance imaging
At this time, breast magnetic resonance imaging (MRI) is not used for routine screening in the general population, and no studies of the effect of screening breast MRI on breast cancer mortality have been published to date. In women at high risk of breast cancer, a comparison of breast MRI and mammography showed that MRI was significantly more sensitive but less specific than mammography. [136, 137, 138, 139] Women who undergo screening with breast MRI must be made aware of the increased risk of a false-positive result that requires additional studies or a biopsy. [137, 140]
Guidelines published by the ACS recommend annual breast MRI (usually in addition to annual mammography) for the following patients:
Women who are carriers of mutations in the BRCA genes or other germline mutation carriers with a known markedly increased risk of breast cancer
First-degree relatives of mutation carriers who have not been tested themselves
Women who have a history of radiation to the breast between the ages of 10 and 30 years
Women with a lifetime risk of breast cancer estimated at 20% or greater according to family history–based risk assessment models (eg, BRCAPro, Myriad, Tyrer-Cusick). 
The ACS guidelines state that additional data are required before making a recommendation for or against screening with breast MRI in those who have a personal history of breast cancer, those with precancerous conditions such as lobular carcinoma in situ (LCIS) or atypical hyperplasia, those with dense breasts, or those who have a 15-20% lifetime risk of breast cancer. MRls are not recommended for those with a lifetime breast cancer risk of less than 15%.
In the United Kingdom, the National Institute for Health and Clinical Excellence (NICE) also issued guidelines for screening with breast MRI. These guidelines suggest annual MRI be done for the following women  :
Age 30–49 years who have not had genetic testing but have a greater than 30% probability of being a BRCA carrier
Age 30–49 years with a known BRCA1 or BRCA2 mutation
Age 20–49 years who have not had genetic testing but have a greater than 30% probability of being a TP53 carrier
Age 20–49 years with a known TP53 mutation.
The Papanicolaou (Pap) smear is the standard screening test for cervical cancer. HPV is the etiologic agent for most cervical cancers, and HPV testing may be used in combination with Pap smear for screening.
This test consists of sampling and examination of the cells at the transformation zone at the junction between the endocervix and ectocervix, which is the site of cervical dysplasia and cancers.
The efficacy of the Pap smear has never been evaluated in a randomized clinical trial, although an observational study in Canada showed a decrease in cervical and uterine cancer mortality rates in areas with high screening rates by Pap smear; areas with low rates showed an increase in mortality from these cancers. 
As the use of Pap smears to screen for cervical cancer became implemented internationally, many other countries reported corresponding declines in cervical cancer incidence and mortality. [144, 145, 146, 147, 148, 149, 150, 151] In addition, a case-control study found that lack of a Pap smear within the 5 years before a cervical cancer diagnosis conveyed an almost 3-fold increase in risk of invasive cancer. 
Two methods of Pap smears are in current use: the conventional smear and liquid-based cytology. The performances of these tests are similar for identifying high-grade squamous lesions with the potential to develop into cancer. [153, 154, 155, 156, 157, 158, 159] Low-grade lesions and atypical squamous or glandular cells are better detected by the liquid-based technique, [160, 161, 162, 163, 164, 165, 166] and a number of reviews have also found that specimen adequacy is better with the liquid-based cytology, but it is not clear that this result represents a clinically significant benefit. [153, 154, 160, 161, 167] An additional benefit of the liquid-based testing is that the same specimen may be used for the Pap smear and for HPV testing (see below). Cost and availability of liquid-based testing measures are other factors that figure into the decision of which method to use.
Approximately 6-7% of Pap smears per year are read as abnormal. [168, 169] Sensitivity and specificity of this test vary substantially: estimates of the sensitivity range from 30% to 87%, whereas specificity is reported as 86-100%. 
Human papillomavirus testing
Two types of tests have been developed to identify high-risk types of HPV, the etiologic agent for most cervical cancers. The first type identifies whether any of 14 high-risk HPV types are present. Examples of this type of test include the Hybrid Capture 2 and the Cervista HPV HR test. The second test, as exemplified by the Cervista HPV 16/18 test, detects HPV types 16 and 18, which are responsible for the majority of cervical cancers and high-grade cervical lesions.
HPV testing has been studied alone and in conjunction with Pap smears. This test does have a greater sensitivity than cervical cytology alone; however, its specificity is lower. [171, 172, 173, 174, 175, 176]
Primary HPV testing is not recommended for women younger than 30 years, as the rate of false-positives is higher in this population. Those older than 30 years who undergo primary HPV testing require a Pap smear to follow up a positive HPV result. Consensus guidelines from the Cytopathology Education and Technology Consortium recommend that women with negative Pap smear and negative HPV testing do not require screening for at least 3 years.  Those with a positive HPV test and a negative Pap smear need to repeat both tests in 1 year; if the tests are negative at that time, the women can return to screening every 3 years.
Guidelines for cervical cancer screening are available from the USPSTF, the ACS, and the ACOG. All recommend starting Pap smears at age 21 years. [178, 179, 180] Although previous guidelines recommended that screening start 3 years after the onset of sexual activity, sexual history is not a consideration in current guidelines.
The USPSTF advises stopping screening at age 65 years, in women who have had adequate prior screening and are not otherwise at high risk for cervical cancer. The ACS and ACOG recommend that in women older than 65, screening can be discontinued after either three consecutive negative cytology tests or two negative cytology and HPV tests within 10 years, provided the most recent test was within 5 years.
Women who have undergone total hysterectomy (with removal of the cervix) for benign causes do not need cervical screening; however, those who have a history of cervical or uterine cancer should continue to have routine age-based screening for at least 20 years. Individuals with a history of immunosuppression or diethylstilbestrol (DES) exposure in utero may also require more frequent screening.
Colorectal cancer screening can be performed using a variety of methods; there are a total of 7 testing options recommended by the Multi-Society Task Force, which includes representation from the American Cancer Society, the American College of Radiology, and the US Multi-Society Task Force on Colorectal Cancer.  The screening modalities for colon cancer can be classified into two general categories: stool-based tests and endoscopic or radiologic examinations.
Stool-based tests have the ability to detect early cancers and may detect advanced adenomas. The first of these tests, the guaiac-based fecal occult blood test (gFOBT), has been shown in clinical trials to reduce colon cancer mortality by up to 33% when done on an annual basis. [182, 183, 184, 185, 186] Advantages of this test include its low cost and noninvasive method. However, the specificity of the gFOBT is low, giving the potential for many false-positive results that require additional testing, such as colonoscopy. Patients should avoid nonsteroidal anti-inflammatory drugs (NSAIDs), red meat, and high doses of vitamin C (>250 mg) for 48 hours before and during the testing period, and samples should be collected from 3 consecutive stools.
More recently, immunochemical-based FOBTs (also known as fecal immunochemical tests) and the stool DNA panel have also become available. The cost of the immunochemical test is greater than that of the guaiac-based test, but the specificity may be higher. Stool DNA panels are also expensive and require a greater quantity of stool to perform the test. The suggested screening interval is every 5 years.
Endoscopic and radiographic tests
Studies that image the colon and rectum have the potential to detect not only cancers but adenomatous polyps that may develop into cancers. Endoscopic tests such as flexible sigmoidoscopy and colonoscopy have been in use as screening tools for many years. Although clinical trials have not addressed the effect of these endoscopic modalities on colorectal cancer mortality in the general population, observational studies have shown that flexible sigmoidoscopy may significantly reduce deaths from colorectal cancers that occur in the area visualized by this scope. [187, 188, 189]
The major limitation of flexible sigmoidoscopy is that it visualizes only the distal 60 cm of the colon. Abnormal results require examination of the entire colon by colonoscopy. The recommended screening interval for flexible sigmoidoscopy is every 5 years. Colonoscopy, however, requires significant bowel preparation and carries the risk of complications such as bleeding or bowel perforation. If there is no evidence of polyps, colonoscopy is repeated every 10 years for screening.
Double-contrast barium enema has also been included as a colon cancer screening option. Although this test is a safe means to visualize the entire bowel, its sensitivity is poor and positive results require additional evaluation with colonoscopy. The most recent USPSTF recommendations do not consider barium enema for colon cancer screening. In the absence of an abnormal result, barium enema is recommended to be performed every 5 years.
Computed tomography (CT) colonography, formerly referred to as “virtual colonoscopy,” has been a more recent development. Similar to optical colonoscopy, this modality visualizes the entire bowel and requires a bowel preparation; however, CT colonography does not pose the risks of complications associated with optical colonoscopy. Positive results require colonoscopy to obtain a biopsy. There is also a risk associated with the cumulative radiation exposure for this test, which could become significant if it is performed regularly for screening. CT colonography should be performed every 5 years.
Several different groups have produced guidelines for colorectal cancer screening. All of the tests listed above are endorsed by the Multi-Society Task Force.  This group encourages physicians and patients to discuss the screening options in terms of early detection (stool-based tests) or prevention (radiographic or endoscopic tests), and then to select a test within the chosen category. Screening is recommended to start at age 50 years in individuals who are at average risk of colon cancer and to continue until the patient’s life expectancy is less than 10 years. However, in 2018 the ACS recommended that colorectal screening begin at age 45 in persons at average risk, in part because of data showing an increase in colorectal cancer in younger populations. 
The recommendations of the American College of Gastroenterology differ in several respects.  Although no preference for screening modality is espoused by the Multi-Society Task Force, the American College of Gastroenterology prefers colonoscopy and fecal immunochemical testing as well as recommends starting screening in black individuals at age 45 years rather than 50 years. The USPSTF guidelines prefer 3 screening strategies: FOBT every year, colonoscopy every 10 years, or the combination of flexible sigmoidoscopy every 5 years and FOBT every 3 years.  The age range put forward for screening in these guidelines is age 50-75 years.
Individuals who are at increased risk of colon cancer due to a personal history of polyps, inflammatory bowel disease (IBD), or previous colorectal cancer or a family history of colorectal cancer should have screening by colonoscopy. The age at which screening is initiated may also be earlier for these individuals, based on the youngest age at which a family member was diagnosed with colorectal cancer or the time of onset of symptoms from inflammatory bowel disease. The examinations should be performed more frequently in these individuals as well, with annual colonoscopy recommended for those at genetic risk and colonoscopy every 1-2 years for those with inflammatory bowel disease. For individuals with a first-degree relative with colorectal cancer but no evidence of a genetic syndrome, screening should start at age 40 years and be repeated every 5 years.
Individuals with a personal history of adenoma should have repeat colonoscopy 3-5 years after the polyp has been removed, with the interval determined on the basis of the histology and number of polyps identified. For very large polyps that may not have been completely resected, short-term repeat colonoscopy several months later may be appropriate. Subsequent intervals for colonoscopy should be 5-10 years in individuals with polyps. For those with a personal history of colon cancer, colonoscopy should be repeated 1 year after cancer diagnosis, then in 1-3 years (based on findings at the 1-year colonoscopy). If no further pathology is identified, colonoscopy should continue at intervals of no more than 5 years for subsequent screening. 
Studies of endometrial cancer screening are lacking; however, on the basis of expert opinion, this screening is not recommended for the general population.  Cervical cytology is not sensitive enough to be a reliable screening test for endometrial cancer, although it is effective in detecting pathology of the squamous cells of the cervix, [195, 196, 197, 198, 199] and endometrial biopsy is an invasive procedure that often does not result in an adequate specimen. In addition, the benefit from presymptomatic diagnosis of endometrial cancer is unclear, as the majority of cancers present as dysfunctional uterine bleeding (DUB) and are diagnosed while still confined to the uterus (stage I).
Women who are at increased hereditary risk of endometrial cancer from Lynch syndrome (hereditary nonpolyposis colorectal cancer [HNPCC]) or from Cowden syndrome are recommended to undergo annual endometrial biopsy starting at age 35 years.  Transvaginal ultrasonography has also been recommended for this group, although some evidence suggests that this procedure is not effective in early detection of cancers. 
Guidelines on lung cancer screening have been issued by the ACS, the American College of Chest Physicians (ACCP), and the USPSTF. [201, 202, 203] The guidelines are in agreement that annual screening with low-dose, computed tomography (LDCT) scanning should be offered to patients aged 55 to 74 years who have at least a 30 pack-year smoking history and either continue to smoke or have quit within the past 15 years. The guidelines also agree that the shared decision making is required and should include a discussion of benefits and risks.
Detection of early stage ovarian cancer has proved difficult: unfortunately, three quarters of ovarian cancers show spread beyond the ovary at the time of diagnosis. Although current guidelines do not recommend screening for ovarian cancer for women in the general population, [204, 205, 206] screening tests such as the serum biomarker CA125 and transvaginal ultrasonography are frequently used in combination to monitor women who are at increased risk of ovarian cancer due to genetic mutations in BRCA or mismatch repair genes. 
Serum CA125 levels have fair sensitivity for advanced ovarian cancer but poor specificity.  A small proportion of healthy women have elevated CA125 levels, and these levels can also be affected by age, smoking status, the menstrual cycle, endometriosis, cirrhosis, fibroids, pelvic inflammatory disease (PID), pleural or peritoneal fluid, or other types of cancers. [208, 209, 210, 211, 212, 213, 214] A change in CA125 level over time may be a more effective means of assessing for ovarian neoplasms.
A panel of serum proteins, including CA125, was marketed in the US as a screening test for ovarian cancer under the brand name OvaSure. However, this test was designed for a population that had a much higher prevalence of ovarian cancer than that of the general population in the US.  Concerns about the validity of this test in the general population led to its removal from the market.
The main imaging modality that has been evaluated for ovarian cancer screening is transvaginal ultrasonography. Although its specificity is good, the sensitivity of screening with this modality varies significantly based on the experience of the operator. [207, 216, 217] Clinical trials to determine whether transvaginal ultrasonography can diagnose early stages of ovarian cancer have had conflicting results. In the National Ovarian Cancer Early Detection Program, all cancers detected in high-risk women were stage III.  However, other studies conducted in lower-risk populations did have a significant proportion of early disease among the cancers detected. [219, 220, 221]
The effects of screening on the early detection and mortality rates of ovarian cancer in women at average risk are being assessed in 3 large, randomized, controlled trials. [219, 222, 223] Each of these studies involves multimodal screening with both transvaginal ultrasonography and serum CA125 testing, with transvaginal ultrasonography or usual care as control groups.
Because of the higher prevalence of ovarian cancer in women at high risk, the predictive value of screening is higher in this population; therefore, some expert groups do endorse screening of high-risk women. However, the National Comprehensive Cancer Network (NCCN) advises that current data do not support routine ovarian cancer screening; transvaginal ultrasound has not been shown to be sufficiently sensitive or specific, but may be considered at the clinician’s discretion starting at age 30–35 y, and similar caveats apply to serum CA-125 testing. 
The mainstays of prostate cancer screening are measurement of prostate-specific antigen (PSA) and digital rectal examination (DRE). PSA testing originated as a tumor marker to assess recurrence or disease progression for men with a history of prostate cancer; however, it was adopted for screening in the general population before this use was evaluated in randomized trials. Later studies had mixed results: the European Randomized Study of Screening for Prostate Cancer (ERSPC) found a survival benefit associated with PSA screening, whereas the PLCO study did not find a benefit associated with screening by PSA and digital rectal examination. [225, 226] Measurement of PSA can be affected by factors other than prostate cancer, including the following [227, 228, 229] :
Prostate biopsy has also been shown to cause significant elevations in PSA sustained for up to 1 month, whereas digital rectal examination is not felt to have a substantive effect on PSA measurements. [230, 231] Overall, when abnormal PSA values are defined as those over 4.0 ng/mL, the sensitivity of the PSA test is 70-80% and the specificity is 60-70%.  A noteworthy exception is the Prostate Cancer Prevention Trial, which showed a sensitivity of 21% for PSA at this level. 
Several approaches have been taken to try to improve the utility of PSA measurement, including use of PSA velocity to assess change over time, PSA density to adjust values according to prostate volume as measured by ultrasonography or MRI, the ratio of free to total PSA, and complexed PSA, as well as individualized reference ranges based on age or race. However, these modified values have not replaced standard PSA testing in most practices.
Despite the long-standing use of digital examination of the prostate through the rectum (ie, digital rectal examination), there have been no controlled studies that demonstrated an effect of this test on prostate cancer mortality or incidence.  Assessment of the prostate by this technique often results in inconsistent results, even among specialists.  The sensitivity has been estimated at 59% and the specificity at 94%.  Clinically, the overall sensitivity is improved when digital rectal examination and PSA are used in combination, although PSA appears to outperform digital rectal examination in some aspects. [194, 237, 238]
Guidelines regarding screening for prostate cancer with PSA testing and digital rectal examination vary considerably. Several groups, including the ACS and the American Urological Association (AUA), recommend discussion of the risks and benefits of screening with the patient and individualizing decisions. [239, 240] For men at average risk, the ACS recommends consideration of starting screening at age 50 years, while the AUA recommends considering starting at age 55 years. For men who are at increased risk of prostate cancer due to family history or ethnic background, the ACS recommends starting at age 45 years. The regimen consists of annual PSA testing, with digital rectal examination optional.
If screening does not detect cancer, the ACS recommends that the time between subsequent screenings depend on the results of the PSA level, as follows  :
At present, 2 medications are available for the primary prevention of breast cancer: tamoxifen and raloxifene. These drugs are selective estrogen receptor modulators (SERMs) that have both estrogen agonist and antagonist effects.
The Breast Cancer Prevention Trial (BCPT) found that, compared with patients receiving placebo, tamoxifen users had a 50% reduction in the incidence of invasive and noninvasive estrogen receptor–positive breast cancers. The investigators evaluated the use of tamoxifen for the prevention of breast cancer in women at increased risk based on age older than 60 years, personal history of lobular carcinoma in situ, or a 5-year Gail score of more than 1.66%.  On long-term follow-up, the protective effect of tamoxifen persisted, with approximately 43% reduction in invasive cancer risk.  However, tamoxifen was also shown to produce an approximately 2-fold increased risk of endometrial cancer and thromboembolic events, including stroke.
A second study, the International Breast Cancer Intervention Study (IBIS-l), also found a significant reduction in the incidence of breast cancer in tamoxifen users, but the all-cause mortality rate was higher in the tamoxifen intervention group.  A meta-analysis concluded that use of tamoxifen reduced breast cancer risk by 38% and doubled the risk of endometrial cancer and thromboembolic events, but it did not affect overall mortality. 
The USPSTF does not recommend use of tamoxifen for chemoprevention of breast cancer in women of average risk. For those who have an increased risk due to family history, BRCA or other mutation carrier status, or conditions such as lobular carcinoma in situ, the benefits of treatment must be balanced against the risks of side effects on an individual basis. 
In the study of tamoxifen and raloxifene (STAR) trial, in which raloxifene (Evista) was compared with tamoxifen for prevention of breast cancer in postmenopausal women, the incidence rates for invasive breast cancer were similar with both drugs, but the risks of thromboembolic adverse effects and endometrial cancer were significantly lower with raloxifene.  In addition, although the rate of noninvasive breast cancer was higher in the raloxifene group than in the tamoxifen group, this difference did not achieve statistical significance. The profile of other side effects also differed between the 2 groups: tamoxifen was associated with higher rates of gynecologic problems, vasomotor symptoms, and bladder symptoms, whereas sexual dysfunction, musculoskeletal issues, and weight gain were more frequent with raloxifene. 
The US Food and Drug Administration (FDA) approved raloxifene for use for breast cancer chemoprevention in postmenopausal women. It is important to note that this drug has not been studied in premenopausal women and is not approved for use in this population. To date, there are no reports on the use of raloxifene in BRCA mutation carriers.
Human papillomavirus (HPV) is a common virus that infects epithelial tissue. More than 120 HPV types have been identified. Most HPV types infect cutaneous epithelial cells and causde common warts (eg, those that occur on the hands and feet). Approximately 40 HPV types infect mucosal epithelial cells on the genitals, mouth, and throat.
Most HPV infections are asymptomatic and resolve spontaneously or become undetectable, but some HPV infections can persist an lead to cancer. Persistent infections with oncogenic HPV types can cause cancers of the anus, cervix, penis, vulva, vagina, and oropharynx. The most common oncogenic HPV types are 16 and 18, which are associated with 70% of cervical cancers and 90% of genital warts.  An estimated 17,600 women and 9,300 men are diagnosed annually in the United States with a cancer caused by HPV. 
Earlier HPV vaccines—Cervarix, which covered two viral types, and Gardasil, which covered four types—were discontinued in the United States in October 2016. The currently available HPV vaccine, Gardasil 9, covers nine HPV types. The FDA-approved indications for Gardasil 9 are shown in Table 1, below.
Table 1. HPV Vaccine (Open Table in a new window)
Anal cancer caused by HPV types 16, 18, 31, 33, 45, 52, and 58
Genital warts (condyloma acuminata) caused by HPV types 6 and 11
Prevention of the following precancerous or dysplastic lesions (ie, anal intraepithelial neoplasia grades 1, 2, and 3)
The nine-valent HPV vaccine is given in either 3 doses over a 6-month period or, in young adolescents, 2 doses over a 6- to 12-month period (see Table 2). The vaccine has been shown to be very effective in the prevention of cervical intraepithelial neoplasia (CIN) grade 2/3 in subjects who had not been previously exposed to HPV. However, the vaccine did not show strong efficacy in preventing premalignant or malignant cervical disease in subjects who were not HPV-naive; nor did the vaccine show efficacy in the treatment of existing HPV infections. [250, 252]
Table 2. HPV Vaccine Dose Schedules (Open Table in a new window)
2-dose series at 0 and 6-12 months*
3-dose series at 0, 2, and 6 months
*For the 2-dose series, if the second dose is administered earlier than 5 months after the first dose, administer a third dose at least 4 months after the second dose
The most frequent adverse effect associated with vaccination was a mild reaction at the injection site. [250, 252] Postlicensure surveillance reports for Gardasil also indicated increased risk of postvaccination syncope and thromboembolic events; however, nearly all thromboembolic events occurred in those with a known risk factor, such as oral contraceptive use or family history of thromboembolic disease. 
Because cervical cancers can be caused by HPV genotypes other than those contained in the vaccines, cervical screening with Pap smears should be continued after vaccination. In addition, the duration of protection against HPV after vaccination remains unknown.
Several groups have made recommendations regarding the appropriate use of HPV vaccinations. The Advisory Committee on Immunization Practices (ACIP) and the American Cancer Society advise routine vaccination for boys and girls at age 11-12 y. [251, 254] The American College of Obstetricians and Gynecologists recommends that vaccination should be offered to girls before their becoming sexually active (at age 13-15 y).  The WHO recommends vaccinations for girls between the ages of 9 and 13 years. 
All groups advocate “catch-up” vaccination for children and young adults between the ages of 13 and 26 years if they have not had previous vaccination, and they indicate that vaccination may occur as early as age 9 years, particularly with children who have a history of sexual abuse or assault. HPV testing is not recommended before vaccination. Additionally, adults not previously vaccinated should be educated about the benefit of the vaccine. The 9-valent HPV vaccine is indicated for males and females aged 9 through 45 years. 
HPV vaccination has not been studied in immunosuppressed or immunocompromised individuals; therefore, at this time, vaccination is not specifically recommended for those in this group. The prescribing information warns that immunosuppressive therapies (eg, irradiation, antimetabolites, alkylating agents, cytotoxic drugs, and corticosteroids [used in greater than physiologic doses]), may reduce the immune responses to vaccines.
5-alpha reductase inhibitors have been shown to have protective effects against prostate cancer in clinical trials. Meta-analysis of 5-alpha reductase inhibitor studies indicates that these agents decrease the risk of prostate cancer by approximately 25%. 
The Prostate Cancer Prevention Trial (PCPT), which compared finasteride to placebo in nearly 19,000 men who were at increased risk of prostate cancer due to age, ethnic background, or family history of prostate cancer, was closed early due to a 25% decrease in numbers of prostate cancer in the finasteride group relative to the control group. However, the finasteride group was noted to have more aggressive cancers (Gleason score >6). 
Several possible explanations for this result have been presented, including diagnostic bias due to decreased prostate volume in the participants taking finasteride and detection bias due to the effects of finasteride on PSA testing. [260, 261, 262, 263, 264, 265] Finasteride decreases PSA levels by 50% on average. [266, 267, 268]
Side effects included gynecomastia and sexual dysfunction, which was mild and decreased over time. It remains unclear whether finasteride decreases mortality from prostate cancer.
Preliminary results from the REDUCE (REduction by DUtasteride of prostate Cancer Events) trial, which investigated dutasteride, another 5-alpha reductase inhibitor, as a chemopreventive agent for men at increased risk of prostate cancer showed a 23% decrease in prostate cancer incidence in the dutasteride arm, which achieved statistical significance.  Unlike the PCPT trial, the incidence of high-grade cancers was not increased in the REDUCE study. Final results on this study are pending.
Guidelines from the American Society of Clinical Oncology and the American Urologic Association recommend that men discuss the risks and benefits of chemoprevention with these medications with their physicians. 
For individuals at very high risk of cancer, such as those with hereditary genetic predisposition, surgical intervention provides another means of risk reduction. Main examples of surgical management of cancer risk include prophylactic mastectomy in BRCA mutation carriers, prophylactic salpingo-oophorectomy in BRCA carriers and mismatch repair gene mutation carriers, and prophylactic colectomy in individuals with familial adenomatous polyposis (FAP).
Prophylactic mastectomy has been a mainstay of management of BRCA mutation carriers because of their markedly increased risk of breast cancer. The breast cancer risk reduction associated with bilateral prophylactic mastectomy is approximately 90%. [271, 272, 273, 274, 275] Simple or skin-sparing mastectomy techniques are preferred over subcutaneous mastectomy, because the latter technique tends to leave more residual breast tissue with the potential to develop cancer. [276, 277, 278]
Despite the considerable risk reduction associated with this procedure, utilization of prophylactic mastectomy remains far less than that of prophylactic salpingo-oophorectomy. Possible reasons for the discrepancy between the rates of these prophylactic surgeries include lack of data proving survival benefit, concerns about appearance and sexuality following mastectomy, availability of medications that reduce breast cancer risk, and the options of screening modalities that can detect breast cancer at a premalignant or early stage.
Prophylactic salpingo-oophorectomy has primarily been studied in women with BRCA1 or BRCA2 germline mutations, although it is also appropriate for women with Lynch syndrome (hereditary nonpolyposis colorectal cancer) and some other hereditary syndromes. This procedure provides premenopausal BRCA mutation carriers with protection from both ovarian cancer (90-95% risk reduction) and breast cancer (50% risk reduction); for postmenopausal carriers, it provides protection from ovarian cancer only. [279, 280, 281, 282, 283] Even after oophorectomy, however, a small risk of primary peritoneal cancer remains. [284, 285]
Prophylactic gynecologic surgery has been shown to improve overall and cancer-related survival in this population.  Similarly, risk-reducing surgery dramatically decreases the incidence of cancer in the Lynch syndrome population as well. 
For BRCA mutation carriers, experts recommend that bilateral salingo-oophorectomy take place between the ages of 35 and 40 years or after childbearing is complete. The fallopian tubes should be removed as well, due to the increased incidence of fallopian tube carcinoma in this population. Careful pathology review of both the ovaries and fallopian tubes is vital to detect clinically occult cancers, which is reported in approximately 4-8% of women undergoing this procedure. [288, 289, 290]
Prophylactic hysterectomy at the time of oophorectomy remains a point of some debate. For women with Lynch syndrome, the risk of endometrial cancer is also increased, and it is appropriate to remove the uterus at the time of oophorectomy. Although BRCA mutations are not generally felt to increase the risk of endometrial cancer, some data suggest that the incidence of these cancers is higher than would be expected in this population. [291, 292] These results may be due to use of tamoxifen for chemoprevention of breast cancer. Removal of the uterus could allow for more complete removal of the fallopian tubes and as well as use of unopposed estrogen for hormone replacement therapy.
Another issue of debate is the use of hormone replacement therapy after prophylactic oophorectomy, which remains controversial in this population due to the risks of breast cancer. At least one report has found that short-term use of hormone replacement to treat menopausal symptoms after oophorectomy in BRCA carriers did not increase the incidence of cancers.  However, long-term follow-up data are lacking, so careful counseling regarding the risks and benefits of hormone replacement therapy is appropriate.
Individuals with the hereditary syndrome familial adenomatous polyposis are often afflicted with hundreds to thousands of colorectal polyps and have a virtual certainty of developing colorectal cancer in their lifetime if their disease is unchecked. A standard risk-reducing measure in this population is prophylactic colectomy, which is generally undertaken at the appearance of adenomas in known mutation carriers. Depending on the phenotype of the individual and other affected members of the family, surgical options include total proctocolectomy with ileal pouch and anastomosis, total abdominal colectomy with ileorectal anastomosis, or total proctocolectomy with ileostomy. For individuals who have an intact rectum after surgery, regular lower endoscopic surveillance is still recommended; similarly, surveillance of the ileal pouch should occur every 2 years in individuals who have undergone this surgical option. [294, 295]
Although the burden of cancer is daunting, primary and secondary prevention of this disease is possible in many instances. Recent trends for decreased cancer incidence and mortality in the US are largely due to improvements in risk reduction measures and early detection of cancer through screening.
Cancer. Fact Sheet No 297. World Health Organization. Available at http://www.who.int/mediacentre/factsheets/fs297/en/. 12 September 2018; Accessed: October 18, 2018.
Edwards BK, Noone AM, Mariotto AB, Simard EP, Boscoe FP, Henley SJ, et al. Annual Report to the Nation on the status of cancer, 1975-2010, featuring prevalence of comorbidity and impact on survival among persons with lung, colorectal, breast, or prostate cancer. Cancer. 2014 May 1. 120 (9):1290-314. [Medline]. [Full Text].
Gail MH, Brinton LA, Byar DP, Corle DK, Green SB, Schairer C. Projecting individualized probabilities of developing breast cancer for white females who are being examined annually. J Natl Cancer Inst. 1989 Dec 20. 81(24):1879-86. [Medline].
Reulen RC, Frobisher C, Winter DL, et al. Long-term risks of subsequent primary neoplasms among survivors of childhood cancer. JAMA. 2011 Jun 8. 305(22):2311-9. [Medline].
Cancer Facts & Figures 2018. American Cancer Society. Available at https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2018/cancer-facts-and-figures-2018.pdf. Accessed: October 18, 2018.
Sasco AJ, Secretan MB, Straif K. Tobacco smoking and cancer: a brief review of recent epidemiological evidence. Lung Cancer. 2004 Aug. 45 Suppl 2:S3-9. [Medline].
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Tobacco Smoke and Involuntary Smoking. (83)2004.
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Smokeless tobacco and some tobacco-specific N-nitrosamines. (89)2007.
Plaskon LA, Penson DF, Vaughan TL, Stanford JL. Cigarette smoking and risk of prostate cancer in middle-aged men. Cancer Epidemiol Biomarkers Prev. 2003 Jul. 12(7):604-9. [Medline].
Office of the Surgeon General (US), Office on Smoking and Health (US). The Health Consequences of Smoking. Centers for Disease Control and Prevention; Office of the Surgeon General (US); Office on Smoking and Health (US). 2004. [Medline]. [Full Text].
Samet JM. The 1990 Report of the Surgeon General: The Health Benefits of Smoking Cessation. Am Rev Respir Dis. 1990 Nov. 142(5):993-4. [Medline].
A report of the Surgeon General. The Benefits of Smoking Cessation. US Department of Health and Human Services. 1990. Available at https://profiles.nlm.nih.gov/NN/B/B/C/T/.
Quitting Smoking. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/tobacco/data_statistics/fact_sheets/cessation/quitting/. December 11, 2017; Accessed: October 18, 2018.
Steinberg MB, Greenhaus S, Schmelzer AC, Bover MT, Foulds J, Hoover DR. Triple-combination pharmacotherapy for medically ill smokers: a randomized trial. Ann Intern Med. 2009 Apr 7. 150(7):447-54. [Medline].
Hughes JR, Keely J, Naud S. Shape of the relapse curve and long-term abstinence among untreated smokers. Addiction. 2004 Jan. 99(1):29-38. [Medline].
Gonzales D, Rennard SI, Nides M, et al. Varenicline, an alpha4beta2 nicotinic acetylcholine receptor partial agonist, vs sustained-release bupropion and placebo for smoking cessation: a randomized controlled trial. JAMA. 2006 Jul 5. 296(1):47-55. [Medline].
Jorenby DE, Hays JT, Rigotti NA, Azoulay S, Watsky EJ, Williams KE. Efficacy of varenicline, an alpha4beta2 nicotinic acetylcholine receptor partial agonist, vs placebo or sustained-release bupropion for smoking cessation: a randomized controlled trial. JAMA. 2006 Jul 5. 296(1):56-63. [Medline].
Nides M, Oncken C, Gonzales D, Rennard S, Watsky EJ, Anziano R. Smoking cessation with varenicline, a selective alpha4beta2 nicotinic receptor partial agonist: results from a 7-week, randomized, placebo- and bupropion-controlled trial with 1-year follow-up. Arch Intern Med. 2006 Aug 14-28. 166(15):1561-8. [Medline].
Stapleton JA, Watson L, Spirling LI, Smith R, Milbrandt A, Ratcliffe M. Varenicline in the routine treatment of tobacco dependence: a pre-post comparison with nicotine replacement therapy and an evaluation in those with mental illness. Addiction. 2008 Jan. 103(1):146-54. [Medline].
Aubin HJ, Bobak A, Britton JR, Oncken C, Billing CB Jr, Gong J. Varenicline versus transdermal nicotine patch for smoking cessation: results from a randomised open-label trial. Thorax. 2008 Aug. 63(8):717-24. [Medline]. [Full Text].
Baker TB, Piper ME, Stein JH, Smith SS, Bolt DM, Fraser DL, et al. Effects of Nicotine Patch vs Varenicline vs Combination Nicotine Replacement Therapy on Smoking Cessation at 26 Weeks: A Randomized Clinical Trial. JAMA. 2016 Jan 26. 315 (4):371-9. [Medline]. [Full Text].
Turner E, Jones M, Vaz LR, Coleman T. Systematic Review and Meta-Analysis to Assess the Safety of Buproprion and Varenicline in Pregnancy. Nicotine Tob Res. 2018 Mar 22. [Medline].
Cinciripini PM, Minnix JA, Green CE, Robinson JD, Engelmann JM, Versace F, et al. An RCT with the combination of varenicline and bupropion for smoking cessation: clinical implications for front line use. Addiction. 2018 Apr 21. [Medline].
Rose JE, Behm FM. Combination Varenicline/Bupropion Treatment Benefits Highly Dependent Smokers in an Adaptive Smoking Cessation Paradigm. Nicotine Tob Res. 2017 Aug 1. 19 (8):999-1002. [Medline]. [Full Text].
Armstrong BK, Kricker A. The epidemiology of UV induced skin cancer. J Photochem Photobiol B. 2001 Oct. 63(1-3):8-18. [Medline].
Rosso S, Zanetti R, Martinez C, Tormo MJ, Schraub S, Sancho-Garnier H. The multicentre south European study ‘Helios’. II: Different sun exposure patterns in the aetiology of basal cell and squamous cell carcinomas of the skin. Br J Cancer. 1996 Jun. 73(11):1447-54. [Medline].
Zanetti R, Rosso S, Martinez C, Nieto A, Miranda A, Mercier M. Comparison of risk patterns in carcinoma and melanoma of the skin in men: a multi-centre case-case-control study. Br J Cancer. 2006 Mar 13. 94(5):743-51. [Medline].
Dubin N, Moseson M, Pasternack BS. Sun exposure and malignant melanoma among susceptible individuals. Environ Health Perspect. 1989 May. 81:139-51. [Medline].
Bastiaens MT, Hoefnagel JJ, Bruijn JA, Westendorp RG, Vermeer BJ, Bouwes Bavinck JN. Differences in age, site distribution, and sex between nodular and superficial basal cell carcinoma indicate different types of tumors. J Invest Dermatol. 1998 Jun. 110(6):880-4. [Medline].
Karagas MR, Stannard VA, Mott LA, Slattery MJ, Spencer SK, Weinstock MA. Use of tanning devices and risk of basal cell and squamous cell skin cancers. J Natl Cancer Inst. 2002 Feb 6. 94(3):224-6. [Medline].
Sunbeds, tanning and UV exposure. World Health Organization (WHO). April 2010. Available at http://www.who.int/mediacentre/factsheets/fs287/en/print.html.
Green A, Williams G, Neale R, Hart V, Leslie D, Parsons P. Daily sunscreen application and betacarotene supplementation in prevention of basal-cell and squamous-cell carcinomas of the skin: a randomised controlled trial. Lancet. 1999 Aug 28. 354(9180):723-9. [Medline].
Huncharek M, Kupelnick B. Use of topical sunscreens and the risk of malignant melanoma: a meta-analysis of 9067 patients from 11 case-control studies. Am J Public Health. 2002 Jul. 92(7):1173-7. [Medline].
Dennis LK, Beane Freeman LE, VanBeek MJ. Sunscreen use and the risk for melanoma: a quantitative review. Ann Intern Med. 2003 Dec 16. 139(12):966-78. [Medline].
Gorham ED, Mohr SB, Garland CF, Chaplin G, Garland FC. Do sunscreens increase risk of melanoma in populations residing at higher latitudes?. Ann Epidemiol. 2007 Dec. 17(12):956-63. [Medline].
Martínez ME, Marshall JR, Giovannucci E. Diet and cancer prevention: the roles of observation and experimentation. Nat Rev Cancer. 2008 Sep. 8(9):694-703. [Medline].
Kushi L, Giovannucci E. Dietary fat and cancer. Am J Med. 2002 Dec 30. 113 Suppl 9B:63S-70S. [Medline].
Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Ascherio A, Willett WC. Intake of fat, meat, and fiber in relation to risk of colon cancer in men. Cancer Res. 1994 May 1. 54(9):2390-7. [Medline].
Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Speizer FE. Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. N Engl J Med. 1990 Dec 13. 323(24):1664-72. [Medline].
Norat T, Bingham S, Ferrari P, Slimani N, Jenab M, Mazuir M. Meat, fish, and colorectal cancer risk: the European Prospective Investigation into cancer and nutrition. J Natl Cancer Inst. 2005 Jun 15. 97(12):906-16. [Medline].
Chao A, Thun MJ, Connell CJ, McCullough ML, Jacobs EJ, Flanders WD. Meat consumption and risk of colorectal cancer. JAMA. 2005 Jan 12. 293(2):172-82. [Medline].
Kushi LH, Doyle C, McCullough M, Rock CL, Demark-Wahnefried W, Bandera EV, et al. American Cancer Society Guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J Clin. 2012 Jan-Feb. 62(1):30-67. [Medline].
Feskanich D, Ziegler RG, Michaud DS, Giovannucci EL, Speizer FE, Willett WC. Prospective study of fruit and vegetable consumption and risk of lung cancer among men and women. J Natl Cancer Inst. 2000 Nov 15. 92(22):1812-23. [Medline].
Smith-Warner SA, Spiegelman D, Yaun SS, Adami HO, Beeson WL, van den Brandt PA. Intake of fruits and vegetables and risk of breast cancer: a pooled analysis of cohort studies. JAMA. 2001 Feb 14. 285(6):769-76. [Medline].
Koushik A, Hunter DJ, Spiegelman D, Beeson WL, van den Brandt PA, Buring JE. Fruits, vegetables, and colon cancer risk in a pooled analysis of 14 cohort studies. J Natl Cancer Inst. 2007 Oct 3. 99(19):1471-83. [Medline].
Kavanaugh CJ, Trumbo PR, Ellwood KC. The U.S. Food and Drug Administration’s evidence-based review for qualified health claims: tomatoes, lycopene, and cancer. J Natl Cancer Inst. 2007 Jul 18. 99(14):1074-85. [Medline].
Park Y, Leitzmann MF, Subar AF, Hollenbeck A, Schatzkin A. Dairy food, calcium, and risk of cancer in the NIH-AARP Diet and Health Study. Arch Intern Med. 2009 Feb 23. 169(4):391-401. [Medline]. [Full Text].
Bingham SA, Day NE, Luben R, Ferrari P, Slimani N, Norat T. Dietary fibre in food and protection against colorectal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC): an observational study. Lancet. 2003 May 3. 361(9368):1496-501. [Medline].
Peters U, Sinha R, Chatterjee N, et al. Dietary fibre and colorectal adenoma in a colorectal cancer early detection programme. Lancet. 2003 May 3. 361(9368):1491-5. [Medline].
Alberts DS, Martínez ME, Roe DJ, et al. Lack of effect of a high-fiber cereal supplement on the recurrence of colorectal adenomas. Phoenix Colon Cancer Prevention Physicians’ Network. N Engl J Med. 2000 Apr 20. 342(16):1156-62. [Medline].
Schatzkin A, Lanza E, Corle D, Lance P, Iber F, Caan B. Lack of effect of a low-fat, high-fiber diet on the recurrence of colorectal adenomas. Polyp Prevention Trial Study Group. N Engl J Med. 2000 Apr 20. 342(16):1149-55. [Medline].
Kushi LH, Byers T, Doyle C, Bandera EV, McCullough M, McTiernan A. American Cancer Society Guidelines on Nutrition and Physical Activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J Clin. 2006 Sep-Oct. 56(5):254-81; quiz 313-4. [Medline].
Harvard Report on Cancer Prevention. Volume 1: Causes of human cancer. Cancer Causes Control. 1996 Nov. 7 Suppl 1:S3-59. [Medline].
Colditz GA, Cannuscio CC, Frazier AL. Physical activity and reduced risk of colon cancer: implications for prevention. Cancer Causes Control. 1997 Jul. 8(4):649-67. [Medline].
Dallal CM, Sullivan-Halley J, Ross RK, Wang Y, Deapen D, Horn-Ross PL. Long-term recreational physical activity and risk of invasive and in situ breast cancer: the California teachers study. Arch Intern Med. 2007 Feb 26. 167(4):408-15. [Medline].
Inoue M, Yamamoto S, Kurahashi N, Iwasaki M, Sasazuki S, Tsugane S. Daily total physical activity level and total cancer risk in men and women: results from a large-scale population-based cohort study in Japan. Am J Epidemiol. 2008 Aug 15. 168(4):391-403. [Medline].
Mao Y, Pan S, Wen SW, Johnson KC,. Physical activity and the risk of lung cancer in Canada. Am J Epidemiol. 2003 Sep 15. 158(6):564-75. [Medline].
Colbert LH, Hartman TJ, Tangrea JA, Pietinen P, Virtamo J, Taylor PR. Physical activity and lung cancer risk in male smokers. Int J Cancer. 2002 Apr 10. 98(5):770-3. [Medline].
Thune I, Lund E. The influence of physical activity on lung-cancer risk: A prospective study of 81,516 men and women. Int J Cancer. 1997 Jan 6. 70(1):57-62. [Medline].
Lee IM, Paffenbarger RS Jr. Physical activity and its relation to cancer risk: a prospective study of college alumni. Med Sci Sports Exerc. 1994 Jul. 26(7):831-7. [Medline].
Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003 Apr 24. 348(17):1625-38. [Medline].
Weight Control and Physical Activity. (6)2002.
Adams TD, Gress RE, Smith SC, Halverson RC, Simper SC, Rosamond WD. Long-term mortality after gastric bypass surgery. N Engl J Med. 2007 Aug 23. 357(8):753-61. [Medline].
Seitz HK, Stickel F. Molecular mechanisms of alcohol-mediated carcinogenesis. Nat Rev Cancer. 2007 Aug. 7(8):599-612. [Medline].
Allen NE, Beral V, Casabonne D, Kan SW, Reeves GK, Brown A. Moderate alcohol intake and cancer incidence in women. J Natl Cancer Inst. 2009 Mar 4. 101(5):296-305. [Medline].
Zhang SM, Lee IM, Manson JE, Cook NR, Willett WC, Buring JE. Alcohol consumption and breast cancer risk in the Women’s Health Study. Am J Epidemiol. 2007 Mar 15. 165(6):667-76. [Medline].
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Alcohol Drinking. 1988(44). Available at http://monographs.iarc.fr/ENG/Monographs/vol44/volume44.pdf.
Colditz GA, Egan KM, Stampfer MJ. Hormone replacement therapy and risk of breast cancer: results from epidemiologic studies. Am J Obstet Gynecol. 1993 May. 168(5):1473-80. [Medline].
Steinberg KK, Thacker SB, Smith SJ, Stroup DF, Zack MM, Flanders WD. A meta-analysis of the effect of estrogen replacement therapy on the risk of breast cancer. JAMA. 1991 Apr 17. 265(15):1985-90. [Medline].
Steinberg KK, Smith SJ, Thacker SB, Stroup DF. Breast cancer risk and duration of estrogen use: the role of study design in meta-analysis. Epidemiology. 1994 Jul. 5(4):415-21. [Medline].
Hou N, Hong S, Wang W, Olopade OI, Dignam JJ, Huo D. Hormone Replacement Therapy and Breast Cancer: Heterogeneous Risks by Race, Weight, and Breast Density. J Natl Cancer Inst. 2013 Sep 3. [Medline].
Stefanick ML, Anderson GL, Margolis KL, Hendrix SL, Rodabough RJ, Paskett ED. Effects of conjugated equine estrogens on breast cancer and mammography screening in postmenopausal women with hysterectomy. JAMA. 2006 Apr 12. 295(14):1647-57. [Medline].
Chlebowski RT, Hendrix SL, Langer RD, Stefanick ML, Gass M, Lane D. Influence of estrogen plus progestin on breast cancer and mammography in healthy postmenopausal women: the Women’s Health Initiative Randomized Trial. JAMA. 2003 Jun 25. 289(24):3243-53. [Medline].
Chlebowski RT, Kuller LH, Prentice RL, Stefanick ML, Manson JE, Gass M. Breast cancer after use of estrogen plus progestin in postmenopausal women. N Engl J Med. 2009 Feb 5. 360(6):573-87. [Medline].
Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer statistics, 2009. CA Cancer J Clin. 2009 Jul-Aug. 59(4):225-49. [Medline].
Kaufman Z, Garstin WI, Hayes R, Michell MJ, Baum M. The mammographic parenchymal patterns of women on hormonal replacement therapy. Clin Radiol. 1991 Jun. 43(6):389-92. [Medline].
Greendale GA, Reboussin BA, Slone S, Wasilauskas C, Pike MC, Ursin G. Postmenopausal hormone therapy and change in mammographic density. J Natl Cancer Inst. 2003 Jan 1. 95(1):30-7. [Medline].
McTiernan A, Martin CF, Peck JD, Aragaki AK, Chlebowski RT, Pisano ED. Estrogen-plus-progestin use and mammographic density in postmenopausal women: Women’s Health Initiative randomized trial. J Natl Cancer Inst. 2005 Sep 21. 97(18):1366-76. [Medline].
Wong O, Whorton MD, Foliart DE, Lowengart R. An ecologic study of skin cancer and environmental arsenic exposure. Int Arch Occup Environ Health. 1992. 64(4):235-41. [Medline].
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Preamble. 2006.
Chang MH. Prevention of hepatitis B virus infection and liver cancer. Recent Results Cancer Res. 2014. 193:75-95. [Medline].
Sugimoto K, Kim SR, Kim SK, Imoto S, Tohyama M, Kim KI, et al. Comparison of Daclatasvir and Asunaprevir for Chronic HCV 1b Infection with Telaprevir and Simeprevir plus Peginterferon and Ribavirin, with a Focus on the Prevention of Occurrence and Recurrence of Hepatocellular Carcinoma. Oncology. 2015 Nov. 89 Suppl 2:42-46. [Medline].
Ozoya OO, Sokol L, Dalia S. “EBV-related Malignancies, Outcomes and Novel Prevention Strategies”. Infect Disord Drug Targets. 2015 Nov 19. [Medline].
Busch MP, Glynn SA, Stramer SL, Strong DM, Caglioti S, Wright DJ, et al. A new strategy for estimating risks of transfusion-transmitted viral infections based on rates of detection of recently infected donors. Transfusion. 2005 Feb. 45(2):254-64. [Medline].
Dodd RY, Notari EP 4th, Stramer SL. Current prevalence and incidence of infectious disease markers and estimated window-period risk in the American Red Cross blood donor population. Transfusion. 2002 Aug. 42(8):975-9. [Medline].
Basow D, ed. Hepatitis C and transfusion: A ‘lookback’ primer. Waltham, MA: UpToDate; 2009.
Little RF. AIDS-related non-Hodgkin’s lymphoma: etiology, epidemiology, and impact of highly active antiretroviral therapy. Leuk Lymphoma. 2003. 44 Suppl 3:S63-8. [Medline].
Sung JJ, Tsoi KK, Wong VW, Li KC, Chan HL. Meta-analysis: Treatment of hepatitis B infection reduces risk of hepatocellular carcinoma. Aliment Pharmacol Ther. 2008 Nov 1. 28(9):1067-77. [Medline].
Uemura N, Mukai T, Okamoto S, Yamaguchi S, Mashiba H, Taniyama K. Effect of Helicobacter pylori eradication on subsequent development of cancer after endoscopic resection of early gastric cancer. Cancer Epidemiol Biomarkers Prev. 1997 Aug. 6(8):639-42. [Medline].
Saito K, Arai K, Mori M, Kobayashi R, Ohki I. Effect of Helicobacter pylori eradication on malignant transformation of gastric adenoma. Gastrointest Endosc. 2000 Jul. 52(1):27-32. [Medline].
Wong BC, Lam SK, Wong WM, Chen JS, Zheng TT, Feng RE. Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial. JAMA. 2004 Jan 14. 291(2):187-94. [Medline].
Thomas DB, Gao DL, Ray RM, Wang WW, Allison CJ, Chen FL. Randomized trial of breast self-examination in Shanghai: final results. J Natl Cancer Inst. 2002 Oct 2. 94(19):1445-57. [Medline].
Harvey BJ, Miller AB, Baines CJ, Corey PN. Effect of breast self-examination techniques on the risk of death from breast cancer. CMAJ. 1997 Nov 1. 157(9):1205-12. [Medline].
Newcomb PA, Weiss NS, Storer BE, Scholes D, Young BE, Voigt LF. Breast self-examination in relation to the occurrence of advanced breast cancer. J Natl Cancer Inst. 1991 Feb 20. 83(4):260-5. [Medline].
Woolf SH. The 2009 breast cancer screening recommendations of the US Preventive Services Task Force. JAMA. 2010 Jan 13. 303(2):162-3. [Medline].
[Guideline] Oeffinger KC, Fontham ET, Etzioni R, et al; American Cancer Society. Breast Cancer Screening for Women at Average Risk: 2015 Guideline Update From the American Cancer Society. JAMA. 2015 Oct 20. 314 (15):1599-614. [Medline]. [Full Text].
Chiarelli AM, Majpruz V, Brown P, Thériault M, Shumak R, Mai V. The contribution of clinical breast examination to the accuracy of breast screening. J Natl Cancer Inst. 2009 Sep 16. 101(18):1236-43. [Medline].
Bobo JK, Lee NC, Thames SF. Findings from 752,081 clinical breast examinations reported to a national screening program from 1995 through 1998. J Natl Cancer Inst. 2000 Jun 21. 92(12):971-6. [Medline].
Murphy AM. Mammography screening for breast cancer: a view from 2 worlds. JAMA. 2010 Jan 13. 303(2):166-7. [Medline].
Berry DA, Cronin KA, Plevritis SK, Fryback DG, Clarke L, Zelen M. Effect of screening and adjuvant therapy on mortality from breast cancer. N Engl J Med. 2005 Oct 27. 353(17):1784-92. [Medline].
Elwood M, Cox B, Richardson A. The effectiveness of breast cancer screening by mammography in younger women: correction. Online J Curr Clin Trials. 1994 Mar 31. Doc No 121:[Medline].
Humphrey LL, Helfand M, Chan BK, Woolf SH. Breast cancer screening: a summary of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2002 Sep 3. 137(5 Part 1):347-60. [Medline].
Nystrom L, Andersson I, Bjurstam N, Frisell J, NordenskjOld B, Rutqvist LE. Long-term effects of mammography screening: updated overview of the Swedish randomised trials. Lancet. 2002 Mar 16. 359(9310):909-19. [Medline].
Freedman DA, Petitti DB, Robins JM. On the efficacy of screening for breast cancer. Int J Epidemiol. 2004 Feb. 33(1):43-55. [Medline].
Gøtzsche PC, Nielsen M. Screening for breast cancer with mammography. Cochrane Database Syst Rev. 2006 Oct 18. CD001877. [Medline].
Schopper D, de Wolf C. How effective are breast cancer screening programmes by mammography? Review of the current evidence. Eur J Cancer. 2009 Jul. 45(11):1916-23. [Medline].
Breen N, A Cronin K, Meissner HI, et al. Reported drop in mammography: is this cause for concern?. Cancer. 2007 Jun 15. 109(12):2405-9. [Medline].
Lewin JM, D’Orsi CJ, Hendrick RE, Moss LJ, Isaacs PK, Karellas A. Clinical comparison of full-field digital mammography and screen-film mammography for detection of breast cancer. AJR Am J Roentgenol. 2002 Sep. 179(3):671-7. [Medline].
Skaane P, Hofvind S, Skjennald A. Randomized trial of screen-film versus full-field digital mammography with soft-copy reading in population-based screening program: follow-up and final results of Oslo II study. Radiology. 2007 Sep. 244(3):708-17. [Medline].
Skaane P, Skjennald A. Screen-film mammography versus full-field digital mammography with soft-copy reading: randomized trial in a population-based screening program–the Oslo II Study. Radiology. 2004 Jul. 232(1):197-204. [Medline].
Pisano ED, Gatsonis C, Hendrick E, Yaffe M, Baum JK, Acharyya S. Diagnostic performance of digital versus film mammography for breast-cancer screening. N Engl J Med. 2005 Oct 27. 353(17):1773-83. [Medline].
Skaane P, Young K, Skjennald A. Population-based mammography screening: comparison of screen-film and full-field digital mammography with soft-copy reading–Oslo I study. Radiology. 2003 Dec. 229(3):877-84. [Medline].
Pisano ED, Hendrick RE, Yaffe MJ, Baum JK, Acharyya S, Cormack JB. Diagnostic accuracy of digital versus film mammography: exploratory analysis of selected population subgroups in DMIST. Radiology. 2008 Feb. 246(2):376-83. [Medline]. [Full Text].
[Guideline] Siu AL, U.S. Preventive Services Task Force. Screening for Breast Cancer: U.S. Preventive Services Task Force Recommendation Statement. Ann Intern Med. 2016 Feb 16. 164 (4):279-96. [Medline].
[Guideline] Committee on Practice Bulletins—Gynecology. Practice Bulletin Number 179: Breast Cancer Risk Assessment and Screening in Average-Risk Women. Obstet Gynecol. 2017 Jul. 130 (1):e1-e16. [Medline]. [Full Text].
Canadian Task Force on Preventive Health Care. Breast Cancer (2011). Available at https://canadiantaskforce.ca/guidelines/published-guidelines/breast-cancer/. Accessed: October 19, 2018.
Hofvind S, Vacek PM, Skelly J, Weaver DL, Geller BM. Comparing screening mammography for early breast cancer detection in Vermont and Norway. J Natl Cancer Inst. 2008 Aug 6. 100(15):1082-91. [Medline]. [Full Text].
Qaseem A, Snow V, Sherif K, Aronson M, Weiss KB, Owens DK. Screening mammography for women 40 to 49 years of age: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2007 Apr 3. 146(7):511-5. [Medline].
Recommendations on cancer screening in the European union. Advisory Committee on Cancer Prevention. Eur J Cancer. 2000 Aug. 36(12):1473-8. [Medline].
Moss SM, Cuckle H, Evans A, Johns L, Waller M, Bobrow L. Effect of mammographic screening from age 40 years on breast cancer mortality at 10 years’ follow-up: a randomised controlled trial. Lancet. 2006 Dec 9. 368(9552):2053-60. [Medline].
Salzmann P, Kerlikowske K, Phillips K. Cost-effectiveness of extending screening mammography guidelines to include women 40 to 49 years of age. Ann Intern Med. 1997 Dec 1. 127(11):955-65. [Medline].
Kerlikowske K, Salzmann P, Phillips KA, Cauley JA, Cummings SR. Continuing screening mammography in women aged 70 to 79 years: impact on life expectancy and cost-effectiveness. JAMA. 1999 Dec 8. 282(22):2156-63. [Medline].
Brown ML, Houn F, Sickles EA, Kessler LG. Screening mammography in community practice: positive predictive value of abnormal findings and yield of follow-up diagnostic procedures. AJR Am J Roentgenol. 1995 Dec. 165(6):1373-7. [Medline].
Christiansen CL, Wang F, Barton MB, Kreuter W, Elmore JG, Gelfand AE. Predicting the cumulative risk of false-positive mammograms. J Natl Cancer Inst. 2000 Oct 18. 92(20):1657-66. [Medline].
Zackrisson S, Andersson I, Janzon L, Manjer J, Garne JP. Rate of over-diagnosis of breast cancer 15 years after end of Malmö mammographic screening trial: follow-up study. BMJ. 2006 Mar 25. 332(7543):689-92. [Medline].
Berrington de Gonzalez A, Reeves G. Mammographic screening before age 50 years in the UK: comparison of the radiation risks with the mortality benefits. Br J Cancer. 2005 Sep 5. 93(5):590-6. [Medline]. [Full Text].
Andrieu N, Easton DF, Chang-Claude J, Rookus MA, Brohet R, Cardis E. Effect of chest X-rays on the risk of breast cancer among BRCA1/2 mutation carriers in the international BRCA1/2 carrier cohort study: a report from the EMBRACE, GENEPSO, GEO-HEBON, and IBCCS Collaborators’ Group. J Clin Oncol. 2006 Jul 20. 24(21):3361-6. [Medline].
Narod SA, Lubinski J, Ghadirian P, Lynch HT, Moller P, Foulkes WD. Screening mammography and risk of breast cancer in BRCA1 and BRCA2 mutation carriers: a case-control study. Lancet Oncol. 2006 May. 7(5):402-6. [Medline].
Corsetti V, Houssami N, Ferrari A, Ghirardi M, Bellarosa S, Angelini O. Breast screening with ultrasound in women with mammography-negative dense breasts: evidence on incremental cancer detection and false positives, and associated cost. Eur J Cancer. 2008 Mar. 44(4):539-44. [Medline].
Berg WA, Blume JD, Cormack JB, Mendelson EB, Lehrer D, Bohm-Velez M. Combined screening with ultrasound and mammography vs mammography alone in women at elevated risk of breast cancer. JAMA. 2008 May 14. 299(18):2151-63. [Medline]. [Full Text].
Buchberger W, Niehoff A, Obrist P, DeKoekkoek-Doll P, Dünser M. Clinically and mammographically occult breast lesions: detection and classification with high-resolution sonography. Semin Ultrasound CT MR. 2000 Aug. 21(4):325-36. [Medline].
Warner E, Plewes DB, Hill KA, Causer PA, Zubovits JT, Jong RA. Surveillance of BRCA1 and BRCA2 mutation carriers with magnetic resonance imaging, ultrasound, mammography, and clinical breast examination. JAMA. 2004 Sep 15. 292(11):1317-25. [Medline].
Kriege M, Brekelmans CT, Boetes C, Besnard PE, Zonderland HM, Obdeijn IM. Efficacy of MRI and mammography for breast-cancer screening in women with a familial or genetic predisposition. N Engl J Med. 2004 Jul 29. 351(5):427-37. [Medline].
Warner E, Messersmith H, Causer P, Eisen A, Shumak R, Plewes D. Systematic review: using magnetic resonance imaging to screen women at high risk for breast cancer. Ann Intern Med. 2008 May 6. 148(9):671-9. [Medline].
Leach MO, Boggis CR, Dixon AK, Easton DF, Eeles RA, Evans DG. Screening with magnetic resonance imaging and mammography of a UK population at high familial risk of breast cancer: a prospective multicentre cohort study (MARIBS). Lancet. 2005 May 21-27. 365(9473):1769-78. [Medline].
Lehman CD, Blume JD, Weatherall P, Thickman D, Hylton N, Warner E. Screening women at high risk for breast cancer with mammography and magnetic resonance imaging. Cancer. 2005 May 1. 103(9):1898-905. [Medline].
Saslow D, Boetes C, Burke W, Harms S, Leach MO, Lehman CD. American Cancer Society guidelines for breast screening with MRI as an adjunct to mammography. CA Cancer J Clin. 2007 Mar-Apr. 57(2):75-89. [Medline].
National Institute of Health and Clinical Excellence. Familial breast cancer: classification, care and managing breast cancer and related risks in people with a family history of breast cancer. Available at https://www.nice.org.uk/guidance/cg164. March 2017; Accessed: October 19, 2018.
Cervical cancer screening programs. I. Epidemiology and natural history of carcinoma of the cervix. Can Med Assoc J. 1976 Jun 5. 114(11):1003-12. [Medline].
Johannesson G, Geirsson G, Day N. The effect of mass screening in Iceland, 1965-74, on the incidence and mortality of cervical carcinoma. Int J Cancer. 1978 Apr 15. 21(4):418-25. [Medline].
Cannistra SA, Niloff JM. Cancer of the uterine cervix. N Engl J Med. 1996 Apr 18. 334(16):1030-8. [Medline].
Nieminen P, Kallio M, Hakama M. The effect of mass screening on incidence and mortality of squamous and adenocarcinoma of cervix uteri. Obstet Gynecol. 1995 Jun. 85(6):1017-21. [Medline].
Benedet JL, Anderson GH, Matisic JP. A comprehensive program for cervical cancer detection and management. Am J Obstet Gynecol. 1992 Apr. 166(4):1254-9. [Medline].
Nygard JF, Skare GB, Thoresen SO. The cervical cancer screening programme in Norway, 1992-2000: changes in Pap smear coverage and incidence of cervical cancer. J Med Screen. 2002. 9(2):86-91. [Medline].
Taylor R, Morrell S, Mamoon H, Wain G, Ross J. Decline in cervical cancer incidence and mortality in New South Wales in relation to control activities (Australia). Cancer Causes Control. 2006 Apr. 17(3):299-306. [Medline].
Aklimunnessa K, Mori M, Khan MM, Sakauchi F, Kubo T, Fujino Y. Effectiveness of cervical cancer screening over cervical cancer mortality among Japanese women. Jpn J Clin Oncol. 2006 Aug. 36(8):511-8. [Medline].
Clarke EA, Anderson TW. Does screening by “Pap” smears help prevent cervical cancer? A case-control study. Lancet. 1979 Jul 7. 2(8132):1-4. [Medline].
Sulik SM, Kroeger K, Schultz JK, Brown JL, Becker LA, Grant WD. Are fluid-based cytologies superior to the conventional Papanicolaou test? A systematic review. J Fam Pract. 2001 Dec. 50(12):1040-6. [Medline].
Davey E, Barratt A, Irwig L, Chan SF, Macaskill P, Mannes P. Effect of study design and quality on unsatisfactory rates, cytology classifications, and accuracy in liquid-based versus conventional cervical cytology: a systematic review. Lancet. 2006 Jan 14. 367(9505):122-32. [Medline].
Arbyn M, Bergeron C, Klinkhamer P, Martin-Hirsch P, Siebers AG, Bulten J. Liquid compared with conventional cervical cytology: a systematic review and meta-analysis. Obstet Gynecol. 2008 Jan. 111(1):167-77. [Medline].
Abulafia O, Pezzullo JC, Sherer DM. Performance of ThinPrep liquid-based cervical cytology in comparison with conventionally prepared Papanicolaou smears: a quantitative survey. Gynecol Oncol. 2003 Jul. 90(1):137-44. [Medline].
Moseley RP, Paget S. Liquid-based cytology: is this the way forward for cervical screening?. Cytopathology. 2002 Apr. 13(2):71-82. [Medline].
Noorani HZ, Brown A, Skidmore B, Stuart GC. Liquid-based cytology and human papillomavirus testing in cervical cancer screening. Technology report no 40. 2003.
Karnon J, Peters J, Platt J, Chilcott J, McGoogan E, Brewer N. Liquid-based cytology in cervical screening: an updated rapid and systematic review and economic analysis. Health Technol Assess. 2004 May. 8(20):iii, 1-78. [Medline].
Ronco G, Cuzick J, Pierotti P, Cariaggi MP, Dalla Palma P, Naldoni C. Accuracy of liquid based versus conventional cytology: overall results of new technologies for cervical cancer screening: randomised controlled trial. BMJ. 2007 Jul 7. 335(7609):28. [Medline].
Davey E, d’Assuncao J, Irwig L, Macaskill P, Chan SF, Richards A. Accuracy of reading liquid based cytology slides using the ThinPrep Imager compared with conventional cytology: prospective study. BMJ. 2007 Jul 7. 335(7609):31. [Medline].
Beerman H, van Dorst EB, Kuenen-Boumeester V, Hogendoorn PC. Superior performance of liquid-based versus conventional cytology in a population-based cervical cancer screening program. Gynecol Oncol. 2009 Mar. 112(3):572-6. [Medline].
Lee KR, Darragh TM, Joste NE, et al. Atypical glandular cells of undetermined significance (AGUS): Interobserver reproducibility in cervical smears and corresponding thin-layer preparations. Am J Clin Pathol. 2002 Jan. 117(1):96-102. [Medline].
Bai H, Sung CJ, Steinhoff MM. ThinPrep Pap Test promotes detection of glandular lesions of the endocervix. Diagn Cytopathol. 2000 Jul. 23(1):19-22. [Medline].
Ashfaq R, Gibbons D, Vela C, Saboorian MH, Iliya F. ThinPrep Pap Test. Accuracy for glandular disease. Acta Cytol. 1999 Jan-Feb. 43(1):81-5. [Medline].
Hecht JL, Sheets EE, Lee KR. Atypical glandular cells of undetermined significance in conventional cervical/vaginal smears and thin-layer preparations. Cancer. 2002 Feb 25. 96(1):1-4. [Medline].
Bernstein SJ, Sanchez-Ramos L, Ndubisi B. Liquid-based cervical cytologic smear study and conventional Papanicolaou smears: a metaanalysis of prospective studies comparing cytologic diagnosis and sample adequacy. Am J Obstet Gynecol. 2001 Aug. 185(2):308-17. [Medline].
Mahdavi A, Monk BJ. Vaccines against human papillomavirus and cervical cancer: promises and challenges. Oncologist. 2005 Aug. 10(7):528-38. [Medline].
Kurman RJ, Henson DE, Herbst AL, Noller KL, Schiffman MH. Interim guidelines for management of abnormal cervical cytology. The 1992 National Cancer Institute Workshop. JAMA. 1994 Jun 15. 271(23):1866-9. [Medline].
Nanda K, McCrory DC, Myers ER, Bastian LA, Hasselblad V, Hickey JD. Accuracy of the Papanicolaou test in screening for and follow-up of cervical cytologic abnormalities: a systematic review. Ann Intern Med. 2000 May 16. 132(10):810-9. [Medline].
Cuzick J, Clavel C, Petry KU, Meijer CJ, Hoyer H, Ratnam S. Overview of the European and North American studies on HPV testing in primary cervical cancer screening. Int J Cancer. 2006 Sep 1. 119(5):1095-101. [Medline].
Kim JJ, Wright TC, Goldie SJ. Cost-effectiveness of human papillomavirus DNA testing in the United Kingdom, The Netherlands, France, and Italy. J Natl Cancer Inst. 2005 Jun 15. 97(12):888-95. [Medline].
Denny LA, Wright TC Jr. Human papillomavirus testing and screening. Best Pract Res Clin Obstet Gynaecol. 2005 Aug. 19(4):501-15. [Medline].
Koliopoulos G, Arbyn M, Martin-Hirsch P, Kyrgiou M, Prendiville W, Paraskevaidis E. Diagnostic accuracy of human papillomavirus testing in primary cervical screening: a systematic review and meta-analysis of non-randomized studies. Gynecol Oncol. 2007 Jan. 104(1):232-46. [Medline].
Mayrand MH, Duarte-Franco E, Rodrigues I, Walter SD, Hanley J, Ferenczy A. Human papillomavirus DNA versus Papanicolaou screening tests for cervical cancer. N Engl J Med. 2007 Oct 18. 357(16):1579-88. [Medline].
Hartmann KE, Hall SA, Nanda K, Boggess JF, Zolnoun D. Screening for Cervical Cancer (2002). Agency for Healthcare Research and Quality. Available at http://www.ahrq.gov/downloads/pub/prevent/pdfser/cervcanser.pdf.
Solomon D, Papillo JL, Davey DD. Statement on human papillomavirus DNA test utilization. Cancer Cytopathol. 2009 Jun 25. 117(3):154-6. [Medline].
[Guideline] Saslow D, et al; ACS-ASCCP-ASCP Cervical Cancer Guideline Committee. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. CA Cancer J Clin. 2012 May-Jun. 62 (3):147-72. [Medline]. [Full Text].
ACOG Practice Bulletin: clinical management guidelines for obstetrician-gynecologists. Number 45, August 2003. Cervical cytology screening (replaces committee opinion 152, March 1995). Obstet Gynecol. 2003 Aug. 102(2):417-27. [Medline].
[Guideline] Moyer VA, U.S. Preventive Services Task Force. Screening for cervical cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2012 Jun 19. 156 (12):880-91, W312. [Medline]. [Full Text].
Levin B, Lieberman DA, McFarland B, Smith RA, Brooks D, Andrews KS. Screening and surveillance for the early detection of colorectal cancer and adenomatous polyps, 2008: a joint guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology. CA Cancer J Clin. 2008 May-Jun. 58(3):130-60. [Medline].
Mandel JS, Church TR, Ederer F, Bond JH. Colorectal cancer mortality: effectiveness of biennial screening for fecal occult blood. J Natl Cancer Inst. 1999 Mar 3. 91(5):434-7. [Medline].
Hardcastle JD, Chamberlain JO, Robinson MH, Moss SM, Amar SS, Balfour TW. Randomised controlled trial of faecal-occult-blood screening for colorectal cancer. Lancet. 1996 Nov 30. 348(9040):1472-7. [Medline].
Jørgensen OD, Kronborg O, Fenger C. A randomised study of screening for colorectal cancer using faecal occult blood testing: results after 13 years and seven biennial screening rounds. Gut. 2002 Jan. 50(1):29-32. [Medline].
Kronborg O, Fenger C, Olsen J, Jørgensen OD, Søndergaard O. Randomised study of screening for colorectal cancer with faecal-occult-blood test. Lancet. 1996 Nov 30. 348(9040):1467-71. [Medline].
Faivre J, Dancourt V, Lejeune C, Tazi MA, Lamour J, Gerard D. Reduction in colorectal cancer mortality by fecal occult blood screening in a French controlled study. Gastroenterology. 2004 Jun. 126(7):1674-80. [Medline].
Newcomb PA, Norfleet RG, Storer BE, Surawicz TS, Marcus PM. Screening sigmoidoscopy and colorectal cancer mortality. J Natl Cancer Inst. 1992 Oct 21. 84(20):1572-5. [Medline].
Müller AD, Sonnenberg A. Protection by endoscopy against death from colorectal cancer. A case-control study among veterans. Arch Intern Med. 1995 Sep 11. 155(16):1741-8. [Medline].
Selby JV, Friedman GD, Quesenberry CP Jr, Weiss NS. A case-control study of screening sigmoidoscopy and mortality from colorectal cancer. N Engl J Med. 1992 Mar 5. 326(10):653-7. [Medline].
Nelson R. Begin Colorectal Cancer Screening at Age 45, Says ACS. Medscape Medical News. Available at https://www.medscape.com/viewarticle/897351. May 30, 2018; Accessed: October 19, 2018.
Rex DK, Johnson DA, Anderson JC, Schoenfeld PS, Burke CA, Inadomi JM. American College of Gastroenterology guidelines for colorectal cancer screening 2009 [corrected]. Am J Gastroenterol. 2009 Mar. 104(3):739-50. [Medline].
Screening for colorectal cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2008 Nov 4. 149(9):627-37. [Medline].
Burt RW, Barthel JS, Dunn KB, et al. NCCN clinical practice guidelines in oncology. Colorectal cancer screening. J Natl Compr Canc Netw. 2010 Jan. 8(1):8-61. [Medline].
Smith RA, von Eschenbach AC, Wender R, Levin B, Byers T, Rothenberger D. American Cancer Society guidelines for the early detection of cancer: update of early detection guidelines for prostate, colorectal, and endometrial cancers. Also: update 2001–testing for early lung cancer detection. CA Cancer J Clin. 2001 Jan-Feb. 51(1):38-75; quiz 77-80. [Medline].
Dash RC, Doud LG. Correlation of pap smear abnormalities in endometrial adenocarcinomas (Abstract). Acta Cytologica. 2001. 45:835-9.
Gu M, Shi W, Barakat RR, Thaler HT, Saigo PE. Pap smears in women with endometrial carcinoma. Acta Cytol. 2001 Jul-Aug. 45(4):555-60. [Medline].
Burk JR, Lehman HF, Wolf FS. Inadequacy of papanicolaou smears in the detection of endometrial cancer. N Engl J Med. 1974 Jul 25. 291(4):191-2. [Medline].
Guidos BJ, Selvaggi SM. Detection of endometrial adenocarcinoma with the ThinPrep Pap test. Diagn Cytopathol. 2000 Oct. 23(4):260-5. [Medline].
Schorge JO, Hossein Saboorian M, Hynan L, Ashfaq R. ThinPrep detection of cervical and endometrial adenocarcinoma: a retrospective cohort study. Cancer. 2002 Dec 25. 96(6):338-43. [Medline].
Dove-Edwin I, Boks D, Goff S, Kenter GG, Carpenter R, Vasen HF. The outcome of endometrial carcinoma surveillance by ultrasound scan in women at risk of hereditary nonpolyposis colorectal carcinoma and familial colorectal carcinoma. Cancer. 2002 Mar 15. 94(6):1708-12. [Medline].
[Guideline] Wender R, Fontham ET, Barrera E Jr, Colditz GA, Church TR, Ettinger DS, et al. American Cancer Society lung cancer screening guidelines. CA Cancer J Clin. 2013 Mar-Apr. 63 (2):107-17. [Medline].
[Guideline] Detterbeck FC, Mazzone PJ, Naidich DP, Bach PB. Screening for lung cancer: Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013 May. 143 (5 Suppl):e78S-92S. [Medline].
[Guideline] Moyer VA, U.S. Preventive Services Task Force. Screening for lung cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2014 Mar 4. 160 (5):330-8. [Medline].
[Guideline] Moyer VA, U.S. Preventive Services Task Force. Screening for ovarian cancer: U.S. Preventive Services Task Force reaffirmation recommendation statement. Ann Intern Med. 2012 Dec 18. 157 (12):900-4. [Medline]. [Full Text].
[Guideline] American College of Obstetricians and Gynecologists Committee on Gynecologic Practice. Committee Opinion No. 477: the role of the obstetrician-gynecologist in the early detection of epithelial ovarian cancer. Obstet Gynecol. 2011 Mar. 117 (3):742-6. [Medline]. [Full Text].
[Guideline] Canadian Task Force on Preventive Health Care. Ovarian Cancer. Available at https://canadiantaskforce.ca/guidelines/appraised-guidelines/ovarian-cancer/. 2013; Accessed: October 19, 2018.
Carlson KJ, Skates SJ, Singer DE. Screening for ovarian cancer. Ann Intern Med. 1994 Jul 15. 121(2):124-32. [Medline].
Bast RC Jr, Klug TL, St John E, Jenison E, Niloff JM, Lazarus H. A radioimmunoassay using a monoclonal antibody to monitor the course of epithelial ovarian cancer. N Engl J Med. 1983 Oct 13. 309(15):883-7. [Medline].
Mol BW, Bayram N, Lijmer JG, Wiegerinck MA, Bongers MY, van der Veen F. The performance of CA-125 measurement in the detection of endometriosis: a meta-analysis. Fertil Steril. 1998 Dec. 70(6):1101-8. [Medline].
Zuckerman E, Lanir A, Sabo E, Rosenvald-Zuckerman T, Matter I, Yeshurun D. Cancer antigen 125: a sensitive marker of ascites in patients with liver cirrhosis. Am J Gastroenterol. 1999 Jun. 94(6):1613-8. [Medline].
Devarbhavi H, Kaese D, Williams AW, Rakela J, Klee GG, Kamath PS. Cancer antigen 125 in patients with chronic liver disease. Mayo Clin Proc. 2002 Jun. 77(6):538-41. [Medline].
Sjovall K, Nilsson B, Einhorn N. The significance of serum CA 125 elevation in malignant and nonmalignant diseases. Gynecol Oncol. 2002 Apr. 85(1):175-8. [Medline].
Topalak O, Saygili U, Soyturk M, Karaca N, Batur Y, Uslu T, et al. Serum, pleural effusion, and ascites CA-125 levels in ovarian cancer and nonovarian benign and malignant diseases: a comparative study. Gynecol Oncol. 2002 Apr. 85(1):108-13. [Medline].
Johnson CC, Kessel B, Riley TL, Ragard LR, Williams CR, Xu JL. The epidemiology of CA-125 in women without evidence of ovarian cancer in the Prostate, Lung, Colorectal and Ovarian Cancer (PLCO) Screening Trial. Gynecol Oncol. 2008 Sep. 110(3):383-9. [Medline].
Clarke-Pearson DL. Clinical practice. Screening for ovarian cancer. N Engl J Med. 2009 Jul 9. 361(2):170-7. [Medline].
Bourne TH, Campbell S, Reynolds KM, Whitehead MI, Hampson J, Royston P. Screening for early familial ovarian cancer with transvaginal ultrasonography and colour blood flow imaging. BMJ. 1993 Apr 17. 306(6884):1025-9. [Medline].
Karlan BY, Raffel LJ, Crvenkovic G, Smrt C, Chen MD, Lopez E. A multidisciplinary approach to the early detection of ovarian carcinoma: rationale, protocol design, and early results. Am J Obstet Gynecol. 1993 Sep. 169(3):494-501. [Medline].
Fishman DA, Cohen L, Blank SV, Shulman L, Singh D, Bozorgi K. The role of ultrasound evaluation in the detection of early-stage epithelial ovarian cancer. Am J Obstet Gynecol. 2005 Apr. 192(4):1214-21; discussion 1221-2. [Medline].
Menon U, Gentry-Maharaj A, Hallett R, Ryan A, Burnell M, Sharma A. Sensitivity and specificity of multimodal and ultrasound screening for ovarian cancer, and stage distribution of detected cancers: results of the prevalence screen of the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS). Lancet Oncol. 2009 Apr. 10(4):327-40. [Medline].
van Nagell JR Jr, DePriest PD, Ueland FR, DeSimone CP, Cooper AL, McDonald JM, et al. Ovarian cancer screening with annual transvaginal sonography: findings of 25,000 women screened. Cancer. 2007 May 1. 109(9):1887-96. [Medline].
Tailor A, Bourne TH, Campbell S, Okokon E, Dew T, Collins WP. Results from an ultrasound-based familial ovarian cancer screening clinic: a 10-year observational study. Ultrasound Obstet Gynecol. 2003 Apr. 21(4):378-85. [Medline].
Buys SS, Partridge E, Greene MH, Prorok PC, Reding D, Riley TL. Ovarian cancer screening in the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial: findings from the initial screen of a randomized trial. Am J Obstet Gynecol. 2005 Nov. 193(5):1630-9. [Medline].
Kobayashi H, Yamada Y, Sado T, Sakata M, Yoshida S, Kawaguchi R. A randomized study of screening for ovarian cancer: a multicenter study in Japan. Int J Gynecol Cancer. 2008 May-Jun. 18(3):414-20. [Medline].
[Guideline] Genetic/Familial High-Risk Assessment: Breast and Ovarian. National Comprehensive Cancer Network. Available at http://www.nccn.org/professionals/physician gis/PDF/genetics screening. pdf. Version 2.2019 — July 30, 2018; Accessed: October 19, 2018.
Schroder FH, Hugosson J, Roobol MJ, Tammela TL, Ciatto S, Nelen V. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med. 2009 Mar 26. 360(13):1320-8. [Medline].
Andriole GL, Crawford ED, Grubb RL 3rd, Buys SS, Chia D, Church TR. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med. 2009 Mar 26. 360(13):1310-9. [Medline].
Tchetgen MB, Oesterling JE. The effect of prostatitis, urinary retention, ejaculation, and ambulation on the serum prostate-specific antigen concentration. Urol Clin North Am. 1997 May. 24(2):283-291. [Medline].
Guess HA, Heyse JF, Gormley GJ. The effect of finasteride on prostate-specific antigen in men with benign prostatic hyperplasia. Prostate. 1993. 22(1):31-7. [Medline].
Roehrborn CG, Marks LS, Fenter T, Freedman S, Tuttle J, Gittleman M. Efficacy and safety of dutasteride in the four-year treatment of men with benign prostatic hyperplasia. Urology. 2004 Apr. 63(4):709-15. [Medline].
Yuan JJ, Coplen DE, Petros JA, Figenshau RS, Ratliff TL, Smith DS. Effects of rectal examination, prostatic massage, ultrasonography and needle biopsy on serum prostate specific antigen levels. J Urol. 1992 Mar. 147(3 Pt 2):810-4. [Medline].
Chybowski FM, Bergstralh EJ, Oesterling JE. The effect of digital rectal examination on the serum prostate specific antigen concentration: results of a randomized study. J Urol. 1992 Jul. 148(1):83-6. [Medline].
Brawer MK. Prostate-specific antigen: current status. CA Cancer J Clin. 1999 Sep-Oct. 49(5):264-81. [Medline].
Thompson IM, Ankerst DP, Chi C, Lucia MS, Goodman PJ, Crowley JJ. Operating characteristics of prostate-specific antigen in men with an initial PSA level of 3.0 ng/ml or lower. JAMA. 2005 Jul 6. 294(1):66-70. [Medline].
Krahn MD, Mahoney JE, Eckman MH, Trachtenberg J, Pauker SG, Detsky AS. Screening for prostate cancer. A decision analytic view. JAMA. 1994 Sep 14. 272(10):773-80. [Medline].
Smith DS, Catalona WJ. Interexaminer variability of digital rectal examination in detecting prostate cancer. Urology. 1995 Jan. 45(1):70-4. [Medline].
Hoogendam A, Buntinx F, de Vet HC. The diagnostic value of digital rectal examination in primary care screening for prostate cancer: a meta-analysis. Fam Pract. 1999 Dec. 16(6):621-6. [Medline].
Carroll P, Coley C, McLeod D, Schellhammer P, Sweat G, Wasson J. Prostate-specific antigen best practice policy–part I: early detection and diagnosis of prostate cancer. Urology. 2001 Feb. 57(2):217-24. [Medline].
Catalona WJ, Richie JP, Ahmann FR, Hudson MA, Scardino PT, Flanigan RC. Comparison of digital rectal examination and serum prostate specific antigen in the early detection of prostate cancer: results of a multicenter clinical trial of 6,630 men. J Urol. 1994 May. 151(5):1283-90. [Medline].
[Guideline] Wolf AM, Wender RC, Etzioni RB, Thompson IM, D’Amico AV, Volk RJ, et al. American Cancer Society guideline for the early detection of prostate cancer: update 2010. CA Cancer J Clin. 2010 Mar-Apr. 60 (2):70-98. [Medline].
[Guideline] Early Detection of Prostate Cancer: AUA Guideline. American Urological Association. Available at https://www.auanet.org/education/guidelines/prostate-cancer-detection.cfm. 2013; Accessed: December 28, 2016.
[Guideline] Moyer VA, U.S. Preventive Services Task Force. Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2012 Jul 17. 157 (2):120-34. [Medline].
Prostate Cancer (2014). Canadian Task Force on Preventive Health Care. Available at https://canadiantaskforce.ca/guidelines/published-guidelines/prostate-cancer/. Accessed: October 19, 2018.
Fisher B, Costantino JP, Wickerham DL, Redmond CK, Kavanah M, Cronin WM. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst. 1998 Sep 16. 90(18):1371-88. [Medline].
Fisher B, Costantino JP, Wickerham DL, et al. Tamoxifen for the prevention of breast cancer: current status of the National Surgical Adjuvant Breast and Bowel Project P-1 study. J Natl Cancer Inst. 2005 Nov 16. 97(22):1652-62. [Medline].
Cuzick J, Forbes J, Edwards R, Baum M, Cawthorn S, Coates A. First results from the International Breast Cancer Intervention Study (IBIS-I): a randomised prevention trial. Lancet. 2002 Sep 14. 360(9336):817-24. [Medline].
Cuzick J, Powles T, Veronesi U, Forbes J, Edwards R, Ashley S. Overview of the main outcomes in breast-cancer prevention trials. Lancet. 2003 Jan 25. 361(9354):296-300. [Medline].
[Guideline] Breast Cancer: Medications for Risk Reduction. U.S. Preventive Services Task Force. Available at https://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/breast-cancer-medications-for-risk-reduction. 2013; Accessed: October 19, 2018.
Vogel VG, Costantino JP, Wickerham DL, Cronin WM, Cecchini RS, Atkins JN. Effects of tamoxifen vs raloxifene on the risk of developing invasive breast cancer and other disease outcomes: the NSABP Study of Tamoxifen and Raloxifene (STAR) P-2 trial. JAMA. 2006 Jun 21. 295(23):2727-41. [Medline].
Land SR, Wickerham DL, Costantino JP, Ritter MW, Vogel VG, Lee M. Patient-reported symptoms and quality of life during treatment with tamoxifen or raloxifene for breast cancer prevention: the NSABP Study of Tamoxifen and Raloxifene (STAR) P-2 trial. JAMA. 2006 Jun 21. 295(23):2742-51. [Medline].
Villa LL, Costa RL, Petta CA, Andrade RP, Ault KA, Giuliano AR. Prophylactic quadrivalent human papillomavirus (types 6, 11, 16, and 18) L1 virus-like particle vaccine in young women: a randomised double-blind placebo-controlled multicentre phase II efficacy trial. Lancet Oncol. 2005 May. 6(5):271-8. [Medline].
Markowitz LE, Dunne EF, Saraiya M, Chesson HW, Curtis CR, Gee J, et al. Human papillomavirus vaccination: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2014 Aug 29. 63 (RR-05):1-30. [Medline]. [Full Text].
Harper DM, Franco EL, Wheeler C, et al. Efficacy of a bivalent L1 virus-like particle vaccine in prevention of infection with human papillomavirus types 16 and 18 in young women: a randomised controlled trial. Lancet. 2004 Nov 13-19. 364(9447):1757-65. [Medline].
Slade BA, Leidel L, Vellozzi C, Woo EJ, Hua W, Sutherland A. Postlicensure safety surveillance for quadrivalent human papillomavirus recombinant vaccine. JAMA. 2009 Aug 19. 302(7):750-7. [Medline].
Saslow D, Andrews KS, Manassaram-Baptiste D, Loomer L, Lam KE, Fisher-Borne M, et al. Human papillomavirus vaccination guideline update: American Cancer Society guideline endorsement. CA Cancer J Clin. 2016 Sep. 66 (5):375-85. [Medline]. [Full Text].
ACOG Committee Opinion No. 344: Human papillomavirus vaccination. Obstet Gynecol. 2006 Sep. 108(3 Pt 1):699-705. [Medline].
U.S. Food and Drug Administration. FDA approves expanded use of Gardasil 9 to include individuals 27 through 45 years old. FDA News Release. 2018 Oct 05. Available at https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm622715.htm.
Wilt TJ, MacDonald R, Hagerty K, Schellhammer P, Kramer BS. Five-alpha-reductase Inhibitors for prostate cancer prevention. Cochrane Database Syst Rev. 2008 Apr 16. CD007091. [Medline].
Thompson IM, Goodman PJ, Tangen CM, Lucia MS, Miller GJ, Ford LG. The influence of finasteride on the development of prostate cancer. N Engl J Med. 2003 Jul 17. 349(3):215-24. [Medline].
Cohen YC, Liu KS, Heyden NL, Carides AD, Anderson KM, Daifotis AG. Detection bias due to the effect of finasteride on prostate volume: a modeling approach for analysis of the Prostate Cancer Prevention Trial. J Natl Cancer Inst. 2007 Sep 19. 99(18):1366-74. [Medline].
Lucia MS, Darke AK, Goodman PJ, La Rosa FG, Parnes HL, Ford LG. Pathologic characteristics of cancers detected in The Prostate Cancer Prevention Trial: implications for prostate cancer detection and chemoprevention. Cancer Prev Res (Phila Pa). 2008 Aug. 1(3):167-73. [Medline].
Lucia MS, Epstein JI, Goodman PJ, Darke AK, Reuter VE, Civantos F. Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial. J Natl Cancer Inst. 2007 Sep 19. 99(18):1375-83. [Medline].
Redman MW, Tangen CM, Goodman PJ, Lucia MS, Coltman CA Jr, Thompson IM. Finasteride does not increase the risk of high-grade prostate cancer: a bias-adjusted modeling approach. Cancer Prev Res (Phila Pa). 2008 Aug. 1(3):174-81. [Medline]. [Full Text].
Pinsky P, Parnes H, Ford L. Estimating rates of true high-grade disease in the prostate cancer prevention trial. Cancer Prev Res (Phila Pa). 2008 Aug. 1(3):182-6. [Medline].
Thompson IM, Chi C, Ankerst DP, Goodman PJ, Tangen CM, Lippman SM. Effect of finasteride on the sensitivity of PSA for detecting prostate cancer. J Natl Cancer Inst. 2006 Aug 16. 98(16):1128-33. [Medline].
Trump DL, Waldstreicher JA, Kolvenbag G, Wissel PS, Neubauer BL. Androgen antagonists: Potential role in prostate cancer prevention. Urology. 2001 Apr. 57(4 Suppl 1):64-7. [Medline].
Guess HA, Gormley GJ, Stoner E, Oesterling JE. The effect of finasteride on prostate specific antigen: review of available data. J Urol. 1996 Jan. 155(1):3-9. [Medline].
Andriole GL, Marberger M, Roehrborn CG. Clinical usefulness of serum prostate specific antigen for the detection of prostate cancer is preserved in men receiving the dual 5alpha-reductase inhibitor dutasteride. J Urol. 2006 May. 175(5):1657-62. [Medline].
GlaxoSmithKline. Large, long-term study shows dutasteride reduced prostate cancerrisk in men at increased risk of the disease. GlaxoSmithKline. Available at http://www.gsk.com/media/pressreleases/2009/2009_pressrelease_10047.htm. Accessed: Feb 10, 2010.
Kramer BS, Hagerty KL, Justman S, Somerfield MR, Albertsen PC, Blot WJ. Use of 5-alpha-reductase inhibitors for prostate cancer chemoprevention: American Society of Clinical Oncology/American Urological Association 2008 Clinical Practice Guideline. J Clin Oncol. 2009 Mar 20. 27(9):1502-16. [Medline].
Rebbeck TR, Friebel T, Lynch HT, Neuhausen SL, van ‘t Veer L, Garber JE. Bilateral prophylactic mastectomy reduces breast cancer risk in BRCA1 and BRCA2 mutation carriers: the PROSE Study Group. J Clin Oncol. 2004 Mar 15. 22(6):1055-62. [Medline].
Hartmann LC, Schaid DJ, Woods JE, Crotty TP, Myers JL, Arnold PG. Efficacy of bilateral prophylactic mastectomy in women with a family history of breast cancer. N Engl J Med. 1999 Jan 14. 340(2):77-84. [Medline].
Hartmann LC, Sellers TA, Schaid DJ, Frank TS, Soderberg CL, Sitta DL. Efficacy of bilateral prophylactic mastectomy in BRCA1 and BRCA2 gene mutation carriers. J Natl Cancer Inst. 2001 Nov 7. 93(21):1633-7. [Medline].
Meijers-Heijboer H, van Geel B, van Putten WL, Henzen-Logmans SC, Seynaeve C, Menke-Pluymers MB. Breast cancer after prophylactic bilateral mastectomy in women with a BRCA1 or BRCA2 mutation. N Engl J Med. 2001 Jul 19. 345(3):159-64. [Medline].
Heemskerk-Gerritsen BA, Brekelmans CT, Menke-Pluymers MB, van Geel AN, Tilanus-Linthorst MM, Bartels CC. Prophylactic mastectomy in BRCA1/2 mutation carriers and women at risk of hereditary breast cancer: long-term experiences at the Rotterdam Family Cancer Clinic. Ann Surg Oncol. 2007 Dec. 14(12):3335-44. [Medline].
Hartmann LC, Degnim A, Schaid DJ. Prophylactic mastectomy for BRCA1/2 carriers: progress and more questions. J Clin Oncol. 2004 Mar 15. 22(6):981-3. [Medline].
Pennisi VR, Capozzi A. Subcutaneous mastectomy data: a final statistical analysis of 1500 patients. Aesthetic Plast Surg. 1989. 13(1):15-21. [Medline].
Guillem JG, Wood WC, Moley JF, Berchuck A, Karlan BY, Mutch DG. ASCO/SSO review of current role of risk-reducing surgery in common hereditary cancer syndromes. J Clin Oncol. 2006 Oct 1. 24(28):4642-60. [Medline].
Rebbeck TR, Lynch HT, Neuhausen SL, Narod SA, Van’t Veer L, Garber JE. Prophylactic oophorectomy in carriers of BRCA1 or BRCA2 mutations. N Engl J Med. 2002 May 23. 346(21):1616-22. [Medline].
Kauff ND, Satagopan JM, Robson ME, Scheuer L, Hensley M, Hudis CA. Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2 mutation. N Engl J Med. 2002 May 23. 346(21):1609-15. [Medline].
Metcalfe K, Lynch HT, Ghadirian P, Tung N, Olivotto I, Warner E. Contralateral breast cancer in BRCA1 and BRCA2 mutation carriers. J Clin Oncol. 2004 Jun 15. 22(12):2328-35. [Medline].
Eisen A, Lubinski J, Klijn J, Moller P, Lynch HT, Offit K. Breast cancer risk following bilateral oophorectomy in BRCA1 and BRCA2 mutation carriers: an international case-control study. J Clin Oncol. 2005 Oct 20. 23(30):7491-6. [Medline].
Rebbeck TR, Levin AM, Eisen A, Snyder C, Watson P, Cannon-Albright L. Breast cancer risk after bilateral prophylactic oophorectomy in BRCA1 mutation carriers. J Natl Cancer Inst. 1999 Sep 1. 91(17):1475-9. [Medline].
Olivier RI, van Beurden M, Lubsen MA, Rookus MA, Mooij TM, van de Vijver MJ. Clinical outcome of prophylactic oophorectomy in BRCA1/BRCA2 mutation carriers and events during follow-up. Br J Cancer. 2004 Apr 19. 90(8):1492-7. [Medline].
Finch A, Beiner M, Lubinski J, Lynch HT, Moller P, Rosen B. Salpingo-oophorectomy and the risk of ovarian, fallopian tube, and peritoneal cancers in women with a BRCA1 or BRCA2 Mutation. JAMA. 2006 Jul 12. 296(2):185-92. [Medline].
Domchek SM, Friebel TM, Neuhausen SL, et al. Mortality after bilateral salpingo-oophorectomy in BRCA1 and BRCA2 mutation carriers: a prospective cohort study. Lancet Oncol. 2006 Mar. 7(3):223-9. [Medline].
Schmeler KM, Lynch HT, Chen LM, Munsell MF, Soliman PT, Clark MB. Prophylactic surgery to reduce the risk of gynecologic cancers in the Lynch syndrome. N Engl J Med. 2006 Jan 19. 354(3):261-9. [Medline].
Powell CB. Occult ovarian cancer at the time of risk-reducing salpingo-oophorectomy. Gynecol Oncol. 2006 Jan. 100(1):1-2. [Medline].
Finch A, Shaw P, Rosen B, Murphy J, Narod SA, Colgan TJ. Clinical and pathologic findings of prophylactic salpingo-oophorectomies in 159 BRCA1 and BRCA2 carriers. Gynecol Oncol. 2006 Jan. 100(1):58-64. [Medline].
Dowdy SC, Stefanek M, Hartmann LC. Surgical risk reduction: prophylactic salpingo-oophorectomy and prophylactic mastectomy. Am J Obstet Gynecol. 2004 Oct. 191(4):1113-23. [Medline].
Biron-Shental T, Drucker L, Altaras M, Bernheim J, Fishman A. High incidence of BRCA1-2 germline mutations, previous breast cancer and familial cancer history in Jewish patients with uterine serous papillary carcinoma. Eur J Surg Oncol. 2006 Dec. 32(10):1097-100. [Medline].
Goshen R, Chu W, Elit L, et al. Is uterine papillary serous adenocarcinoma a manifestation of the hereditary breast-ovarian cancer syndrome?. Gynecol Oncol. 2000 Dec. 79(3):477-81. [Medline].
Rebbeck TR, Friebel T, Wagner T, et al. Effect of short-term hormone replacement therapy on breast cancer risk reduction after bilateral prophylactic oophorectomy in BRCA1 and BRCA2 mutation carriers: the PROSE Study Group. J Clin Oncol. 2005 Nov 1. 23(31):7804-10. [Medline].
Church J, Simmang C. Practice parameters for the treatment of patients with dominantly inherited colorectal cancer (familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer). Dis Colon Rectum. 2003 Aug. 46(8):1001-12. [Medline].
Guillem JG, Wood WC, Moley JF, Berchuck A, Karlan BY, Mutch DG. ASCO/SSO review of current role of risk-reducing surgery in common hereditary cancer syndromes. J Clin Oncol. 2006 Oct 1. 24(28):4642-60. [Medline].
Anal cancer caused by HPV types 16, 18, 31, 33, 45, 52, and 58
Genital warts (condyloma acuminata) caused by HPV types 6 and 11
Prevention of the following precancerous or dysplastic lesions (ie, anal intraepithelial neoplasia grades 1, 2, and 3)
2-dose series at 0 and 6-12 months*
3-dose series at 0, 2, and 6 months
Joanne Jeter, MD Assistant Professor of Clinical Medicine, Section of Hematology/Oncology, Department of Medicine, Arizona Health Sciences Center
Joanne Jeter, MD is a member of the following medical societies: American Society of Clinical Oncology
Disclosure: Received grant/research funds from sanofi-aventis for principal investigator.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Wafik S El-Deiry, MD, PhD Rose Dunlap Professor of Medicine, Chief, Division of Hematology and Oncology, Penn State Hershey Medical Center
Wafik S El-Deiry, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society for Clinical Investigation, American Society of Gene and Cell Therapy
Disclosure: Nothing to disclose.
Research & References of Preventive Oncology|A&C Accounting And Tax Services