Prostate-Specific Antigen Screening: Friend or Foe?

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Prostate-Specific Antigen Screening: Friend or Foe?

Morse Linn, BSN, CURN; A. Ball, MD, BA, FACS; Ann Maradiegue, PhD, C-FNP, RN Urol Nurs. 2007;27(6):481-489. ©2007 Society of Urologic Nurses and Associates

Posted 01/09/2008 http://www.medscape.com/viewarticle/568053_print

Abstract and Introduction

Abstract

Prostate cancer is the most frequently diagnosed cancer among men in the United States. The prostate-specific antigen (PSA) blood test is the most commonly utilized test to detect early prostate malignancy. Elevated PSA levels suggest to providers the possibility that their patients are at a higher statistical risk of harboring asymptomatic, organ-confined prostate cancer. Although PSA testing has become a primary screening method for prostate cancer in the United States, this test has come under scrutiny. PSA screening lacks a high level of specificity due to frequent false-positive results. Additionally, major health organizations differ in their screening recommendations for use of the PSA test. However, the medical community, and more importantly, patients, must understand the benefits and possible detriments of this screening test. Providers should approach each man individually when recommending a PSA test, noting that many risk factors must be considered in a screening protocol for prostate cancer.

Introduction

Prostate cancer (PCA) is expected to be the most frequently diagnosed cancer for men in the United States, with an estimated 218,890 new cases anticipated for 2007. The National Cancer Institute expects 27,050 deaths from PCA in 2007 (National Cancer Institute [NCI], 2007). Based on published rates during 2000-2004, one out of every six men will be diagnosed with prostate cancer during their lifetime (NCI, 2006a). The prostate-specific antigen (PSA) blood test has become the screening tool of choice for the detection of prostate cancer in men, since its approval in 1992 by the Food and Drug Administration (Han, Gann & Catalona, 2004). Prior to the discovery of this blood test, the majority of prostate cancers were identified in an advanced and incurable stage. As low-stage prostate cancer has few signs or symptoms, the discovery of a screening test that could identify localized, and potentially curable disease, has been considered a valuable diagnostic tool. PSA has been reported to be an aide in diagnosing early-stage prostate cancer; however, controversy surrounding this screening test exists.

Several authorities question the utility of the PSA blood test as a screening tool for PCA. For example, normal ranges used for PSA values are somewhat arbitrary. There is poor correlation between the serum PSA values and the actual existence of PCA in any individual patient, leading to the potential for the over-diagnosing of insignificant prostate tumors. Even though overall mortality from prostate cancer has clearly improved in the "PSA era," it is still unknown whether this change is a result of increased screening, improved treatment, or other factors. There are two major, ongoing, clinical trials looking at whether PSA screening actually influences PCA mortality (NCI, 2006b; Schroder, 2005). In the meantime, there is no clear consensus on how best to use PSA as a screening test, as evidenced by the fact that several national health organizations differ in their recommendations for PCA screening and the use of PSA.

Many prostate cancers are indolent and pose no threat to life, while others are virulent and life threatening. While all pro state cancers will not cause death, they may cause morbidity (Tanagho & McAninch, 2004). The broad spectrum of this biological activity causes complexity when screening protocols are proposed. The purpose of this article is to review the medical evidence and controversy surrounding PSA screening.

Methodology

Data were obtained from the following sources: Evidence-Based Medicine Reviews, Medline, and CINAHL (1991-2007). Database searches were performed using the terms: prostate-specific antigen, PSA, prostate cancer, prostatectomy, prostatic hyperplasia, prostate cancer screening, and prostate cancer costs. Statistics and research material from government databases were used regarding the prevalence of prostate cancer, the recommendations for screening, and the treatment options.

Prostate-Specific Antigen

PSA is a 27 kilodalton glycoprotein produced by the prostatic epithelium and periurethral glands (Han et al., 2004). It is a serine protease that causes the liquefaction of congealed seminal fluid and is thus a normal product of the prostate gland and normal component of the seminal fluid. Minute amounts of this protein leach into the blood and are detectable quantitatively by a number of chemical assays. Catalona and colleagues (1991) first reported the use of PSA serum levels as a first-line screening tool to detect prostate cancer. These researchers found that a single PSA determination was more accurate than a digital rectal examination (DRE), heretofore, the standard and only method available to detect PCA, and to identify early PCA (Catalona et al., 1991). Evidence followed supporting that a normal serum PSA (sPSA) was defined as less than or equal to 4.0 ng/ml (Catalona, , & Ornstein, 1997). Scientists re ported that 35% to 45% of men with PSA values above this level had a significant prostate cancer (Durkan, Sheikh, , Hil dreth, & Greene, 2002; Han et al., 2004). The sensitivity (a positive test for men with prostate cancer) with a sPSA greater than 4.0 ng/ml was reported as being 67.5% to 80%, while the specificity rate (a negative test for men without disease) was 60% to 70% (Brawer, 1999).

PSA, being a chemical naturally produced in a normal prostate gland, can be excreted into the blood at variable levels, thus causing serum values to vary, even in patients without PCA. Thus, false-positive tests are not uncommon as noted by the relatively low specificity rate. Ascribing the cause of an elevated PSA can be difficult since many factors can cause changes in the serum level. Elevated serum levels of PSA may be indicative of an abnormality with the prostate; however, it is not disease specific (Han et al., 2004). Examples of the etiology of elevated sPSA in the absence of malignancy include benign prostatic hyperplasia, prostatitis, prostatic infarction, physical activity, ejaculation, DRE, other urinary tract infections, urinary retention, prostate surgery, and urethral catheterization.

Consequently, researchers developed additional methods of evaluating the PSA along with other risk factors in the hope of predicting PCA accurately. Re fining PSA has been the goal of research in order to decrease the number of false-positive tests and improve both sensitivity and specificity.

The serial PSA value, or PSA velocity, is a measurement that compares the values of PSA over time. A rise of more than 0.75 ng/ml during a 12-month period, utilizing at least three separate data points, is considered to be suspicious for prostate cancer ( et al., 1992; , Ankerst et al., 2005). and colleagues (2006) proposed that PSA velocity may be more accurate in identifying life-threatening disease than static PSA determinations. These researchers believe that PSA velocity may have the greatest value in predicting potentially mortal prostate malignancies at a curable stage, particularly in younger men ( et al., 2006).

Benign prostatic hyperplasia (BPH) will also produce increased PSA levels. By virtue of age, BPH is very prevalent in men considered at risk for PCA. Therefore, examining the PSA density (the relationship between the prostate volume and serum PSA levels) can reveal information regarding the potential benign or malignant prostate tissue generating the PSA glycoprotein (Tanagho & McAninch, 2004).

Another interesting and poorly understood association is the relationship of PSA found freely circulating in the blood (fPSA) with PSA bound to other serum proteins such as albumin, trypsin, and chymotrypsin. The ratio of free PSA (fPSA) to total PSA (tPSA), which is defined as the amount of both free and bound PSA, has a predictive correlation with the statistical risk of harboring PCA. In men with a tPSA between 4 and 10 ng/ml and a "fPSA/tPSA" ratio greater than 0.25 the PCA risk is 6%; whereas, men with f/t PSA ratios below 10% with similar total PSA values have a PCA risk of 56% (Catalona et al., 1998; Han et al., 2004).

Normal PSA levels appear to change with age. Therefore, the predictive value of elevated PSA in detecting PCA also need to be correlated to age. The "age-adjusted PSA" has thus been suggested for screening (see Table 1 ).

Catalona and colleagues (1997) discovered that initial PSA levels greater than 2.5 ng/ml increase a man's lifetime risk of developing PCA; therefore, he suggests a baseline PSA be obtained at age 40. Men between ages 40 and 49 years have median PSA values ranging from 0.7 to 1.23 ng/dL (Loeb et al., 2006). Parenthetically, it was reported that a static PSA greater than 2.5 ng/mL in a man less than age 50 years was a strong indicator for prostate cancer risk (Loeb et al., 2006).

Age adjustment also applies to older men. Men over 60 years of age have higher reference ranges ( & Oesterling, 1997). Thus, when considering guidelines to evaluate men at risk for PCA, one should note that older men likely have higher serum PSA values than younger men and that higher PSA levels in older men are expected and may be less significant for predicting significant PCA. Finally, PCA is often indolent, requiring 10 years or more from the time of diagnosis to cause morbidity or mortality. Current scientific opinion indicates that men who have a life expectancy of less than 10 years are unlikely to benefit from PCA screening or even treatment of their disease (Walter, Bertenthal, Lindquist, & Konety, 2006).

Screening Recommendations

The American Urological As sociation (AUA) and American Cancer Society (ACS) recommend offering a screening PSA along with a DRE for men age 50 and above who are expected to live longer than 10 years. Men at higher risk, such as African Ameri cans and men with a family history of PCA, should begin testing at age 40 to 45, or 5 years before the age of onset of disease of the affected family member. The DRE is considered an integral part of the screening protocol and is utilized in conjunction with the PSA, according to the AUA and ACS. The sensitivity of diagnosing tumors is markedly improved with the use of both modalities (Coley, Barry, Fleming, & Mulley, 1997).

The diagnosis of PCA is made by pathologic tissue examination based on prostate biopsy. The issue surrounding PCA screening is the indication for recommending a prostate biopsy. Currently, The AUA recommends prostate biopsy for patients with a total serum PSA value of 4.0 ng/dL or greater, a significant PSA velocity change, or any suspicious DRE abnormality (AUA, 2000). This combination of tests for screening allows providers to detect prostate cancer at earlier stages than historical screening modalities (Bill-Axelson et al., 2005).

An inclusive screening program for PCA should also include several other risk factors such as first or second degree relatives with PCA, ethnic background, and diet. These categories of men should begin screening at age 40 (Moul, 2003). There is evidence that a diet high in animal fat may contribute to a higher possibility of cancer (ACS, 2007).

Decision making with regard to offering patients screening is made even more difficult, as several medical organizations vary widely in their recommendations for PSA screening (see Table 2 ).

There is not universal support for mass screening for PCA (Cookson & , 2000). Several studies suggest that PCA screening does not affect disease-specific survival, and that there may be an over-diagnosis of insignificant prostate cancers (Albertsen, Han ley, & Fine, 2005; Schroder, 2005; Walter et al., 2006). Thus, many epidemiologists and health care payers find the current recommendations unacceptable. Screening policy must, therefore, balance financial considerations and scientific rationale (Schroder, 2005). The feasibility of a screening program must meet criteria as an efficacious tool:

Disease must be prevalent and serious enough to require screening. Prostate cancer meets this requirement.

Early, pre-symptomatic disease must be detected by the test. PSA and DRE used together would meet this condition.

Evidence must be present to show that early discovery of the disease will reduce morbidity and/or mortality. This requirement remains un proven and debatable (Cookson & , 2000).

The lead time for PSA screening (the interval of time between laboratory detected disease and clinically detected disease) was estimated at 12.3 years in the European Randomized Study for Screening of Prostate Cancer ( & Crawford, 2004). Lead time may depend upon the patient's age, screening intervals, and treatments used (Schroder, 2005). Since prostate tumors frequently have slow-growing characteristics, screening may lead to over-diagnosis (Kramer, Brown, Prorok, Potosky, & Gohagan, 1993). Early detection of PCA does not necessarily mean that the cancer will cause the patient's death as the patient may die from other causes before the cancer becomes symptomatic (, 2004). Early detection may increase the time that the patient is aware of the disease, without changing the progression or outcome of the disease. Lead-time bias is implied if mortality is not affected by treatment as it appears that screening helps to improve survival ( & Crawford, 2004). PSA screening has been accused of lead-time bias since many of the tumors do not change the time of death. Screening and treatment must be considered together as the cancer that is identified and treated due to screening should lead to reduced mortality rates.

There would be less debate about PCA screening if the morbidity from the various treatments were insignificant. It is encouraging that treatment options for localized disease have improved over the years, resulting in decreased morbidity with active surveillance for watchful waiting, improved surgical techniques, and more accurate delivery of radiation therapy. There have been improvements in quality-of-life issues such as incontinence (sen, , Estey, & Voaklander, 2007). Future studies hope to show continuing improvement in erectile function following surgical treatment. Most important, treatment for localized disease has a very high survival rate of approximately 99% over a 5-year period (, Bermejo, Her nandez, Basler, & Canby-Hagino, 2005). A significant point is the noted reduction in distant metastasis and tumor progression following radical prostatectomy compared to watchful waiting, al though overall mortality rates did not change in this research study (Bill-Axelson et al., 2005).

Epidemiology

There is a genetic component to PCA. For example, men with a first-degree relative with prostate cancer have a two to three times greater risk of developing PCA compared to men without a familial history of disease (American Society of Clinical Oncology [ASCO], 2006). This inherited trait occurs in about 5% of prostate cancers (ASCO, 2006). Early studies of PCA risk focused on linkage studies that were attentive to families with an extensive history of PCA. These early studies suggested that rare, autosomal dominant genes such as the BRCA1, BRCA2 genes in breast cancer, and the APC gene in colon cancer would lead to the discovery of the PCA gene. Researchers have found at least 10 loci for PCA susceptibility; however, followup studies of these genes fail to consistently validate findings (ASCO, 2006; National Institutes of Health [NIH], 2006; Shaid, 2004). More recently, two independent genome wide association studies identified the 8q24 locus with prostate cancer, as well as colon cancer (Haiman et al., 2007; Yeager et al., 2007). There is currently no genetic test available to determine a man's probability of developing prostate cancer based primarily on his genetic code (ASCO, 2006).

African-American men clearly have a higher incidence and mortality rate due to prostate cancer (NIH, 2006). An African-American man is 1.6 times more likely to be diagnosed with PCA as compared to a white man (Jayadevappa, Chhatre, Weiner, Bloom, & Malkowicz, 2005). African-American men often present with a higher stage of cancer and, as a result, die at a younger age (Jayadevappa et al., 2005). There are many factors that may be causing this racial difference. Genetic factors are being studied, but environmental and social factors are also being considered. According to the U.S. Department of Health and Human Services (USDHHS, 2003), African Ameri cans have poorer quality health care and have less access to medical treatment. Data suggest that this racial difference may stem from the fact that fewer African Americans have health insurance and live at a lower socioeconomic level (USDHHS, 2003).

Historically, African-American men have been reluctant to see a physician because of past, abusive, and unethical medical trials, such as the Tuskegee Syphilis Treatment Study (Chan, Haynes, O'Donnell, Bachino, & Vernon, 2003). Fear and embarrassment may accompany the prostate cancer screening since men know that a DRE will be included in that evaluation. Chan and associates (2003) found that African-American men were less receptive to the DRE as they associate the examination with homosexuality. The screening of African-American men should be considered vital due to the impact of the elevated risk of disease in this patient population (Demark-Wahnefried et al., 1995).

PSA Screening Movement

Use of the PSA blood test has become a routine of practice in the United States. The ACS and AUA both recommend PSA and DRE screening for PCA. This has led Medicare to approve payment of one screening PSA test per year. PSA screening is prevalent across the country, as Sirovich, Schwartz, and Woloshin (2003) reported that 75% of men age 50 and older have had a PSA drawn. Of that group of men, 54% stated that they were up to date with the annual test. The momentum for PSA screening has only increased the public demand due to information fed from the medical community, the media, the press, blue ribbon panels, and public figures, such as General Norman Schwarzkopf, Harry Belafonte, and Bob Dole, who speak openly about their experiences with prostate cancer. Recommendations abound that men participate with prostate screening programs. Due to the high prevalence of the disease in the general population, many men are aware of other men, family, friends, or associates, who have had PCA. These men are likely to request screening evaluations from their providers (Sirovich et al., 2003).

Finally, many practitioners will recommend the test for patients due to the "standard of care" practices in their community. Patients' expectations and the medical liability issue weigh heavily on decision making with regard to screening for PCA (Sirovich et al., 2003). The model of shared decision making is recommended as a way for practitioners to guide patients when considering a PSA screening test. This is a complex process that involves the unbiased sharing of information and relies on the patientunderstanding of medical issues (Sheridan, , & Woolf, 2004). This model requires that the practitioner inform the patient of the risks and benefits of having a certain test performed, or not performed. Then together a decision would be made as to the best course of action for the individual patient.

Screening Controversies

So why does controversy exist concerning the use of the PSA blood test as a general screening tool for the early detection of prostate cancer? First, the very researchers who initially reported its efficacy as a tool for detecting significant PCA at an early stage have recently cast doubt on their original opinions of the value and validity of the test. Second, the standard "normal" range of PSA is arbitrary. and colleagues (2004) state that there is no safe reference range for the normal value for PSA. Biopsy-detected cancer has been found in 15% to 20% of men who had PSA levels in the "normal" range of 2.5 to 4.0 ng/ml (Catalona et al., 1997; et al., 2004). That being noted, lowering the acceptable normal PSA values will improve the specificity of the test; however, the selectivity would be altered as the majority of patients with elevated PSA values do not harbor disease. The false-positive rate for an elevated sPSA is approximately 75%, based on pathologic evaluation of tissue obtained by prostate biopsy (Arcangeli, Ornstein, Keetch, & Andriole, 1997).

There is accumulating evidence that not all PSA-detected PCA is significant. The study by Albertsen and colleagues (2005) collected over 15 years, from the time of diagnosis of clinical stage T1c disease, revealed no increase of cancer progression rates for men treated with watchful waiting or hormone therapy than for men treated with surgery or radiation (Albertsen et al., 2005). These authors suggest that men with low-grade disease often will live a long time after their diagnosis without treatment. Con versely, Johansson, a long-time proponent of surveillance only for patients with PCA, abruptly altered his recommendations in a landmark article reported in JAMA (Johansson et al., 2004). Johansson and colleagues (2004) observed that there are unequivocally subsets of patients, screened for and diagnosed with PCA for whom surveillance is not appropriate. In fact, younger men with life expectancy greater than 10 years and harboring less well-differentiated tumors performed much worse in the surveillance group compared to the treated group. Also noted was an increasing morbidity of local and distant complications of untreated PCA as time progressed from the time of diagnosis. Thus, this well-published proponent of watchful waiting only has altered his own course to recommend treatment of high-risk patients.

and Lohr (2002) stated that there is not enough evidence to verify if early detection reduces prostate cancer death. The NCI (2006a) listed several caveats pertaining to the use of PSA as a screening study on their published fact sheet:

PSA may detect slow-growing tumors that may never cause harm. Most men with an abnormal PSA do not have cancer. Cancer may be present in men with normal PSA values.

The United States Pre ventative Services Task Force (USPSTF) concurs with the National Cancer Institute by stating that screening for PCA has possible harmful effects. False-positive results can lead to unnecessary anxiety and biopsy, and that early detection and treatment for insignificant cancer is needless ( & Lohr, 2002). The USPSTF concluded that clinicians should not order screening without discussing all of the possible risks that accompany the PSA test. The Centers for Disease Control and Prevention (CDC, 2006) recommends balanced information be provided to men regarding the pros and cons of screening. Their decision guide states that the medical experts are unclear if the benefits of screening outweigh the known side effects of treatment (CDC, 2006). Thus, providers are left in a quagmire (see Case Study).

Financial Considerations

Treating prostate cancer has direct and indirect costs. The direct health care costs include physician services, hospitalization, medications, and home health care. Indirect costs include loss of productivity from work, time spent dealing with the illness, transportation, household help, education, medical supplies, and long-term care of the disease and complications of treating the disease (Max et al., 2002). Due to the prevalence of the disease and the aging population of men, the annual cost of treating PCA will grow to several billion dollars per year (Jayadevappa et al., 2005). The treatment of PCA was found to cost approximately $35,000 per case when all treatment options including all stages of cancer were calculated for the year 2000 (Ruchlin & Pellissier, 2001). The costs of PCA will rise as men live longer and screening continues. Medicare will be required to cover the large amount of these costs for the elderly. The cost effectiveness of screening has been difficult to calculate due to the uncertainties about the benefits of the PSA test ( & Lohr, 2002).

Psychological Effects

The psychological effect of PCA screening also deserves consideration. Pain, suffering, and psychological distress should be included as associated costs of the treatment (Max et al., 2002). Men may experience high levels of anxiety while awaiting results from testing (NCI, 2006c). This anxiety may enter the day-to-day affairs and affect work or personal relationships. The impact of a cancer diagnosis is life changing. The impact of false-positive screening tests is also significant. "Anxiety associated with cancer may increase feelings of pain, interfere with one's ability to sleep, cause nausea and vomiting, and interfere with the patient's quality of life" (Dana Farber Cancer Institute, 2006, para. 1). Following the receipt of a diagnosis of prostate cancer, a patient will enter into a category from which he cannot escape. From the time the diagnosis is given to the patient, he has cancer, indolent or not, and he is filled with profound fear and dread. This very point makes the option of watchful waiting difficult for many men as they may not be comfortable "not treating" their cancer. Additionally, pressure to act is often encouraged by well-intentioned, but under-informed family members and friends who argue to actively "fight the cancer." Men with prostate cancer also often wish to begin aggressive treatment as soon as possible to avoid the associated morbidity and possible mortality caused by prostate cancer without full knowledge of the disease's potential course.

Conclusion

The current inconsistencies with regard to the recommendations for using the PSA blood test as a screening tool for prostate cancer screening leaves practitioners with many questions. Evidence-based outcomes data are often interpreted differently by different authorities. Ongoing debate will continue in editorials, journal articles, and, unfortunately, by the tort bar. Table 3 summarizes the multiple issues that surround this debate. There does not appear to be one right or wrong answer for the query: Screening: Friend or Foe?"

and colleagues (2006) developed a risk calculator that computes factors to determine if prostate biopsy should be recommended. A patient or practitioner enters the required values and receives a probability number regarding suspicion for cancer. The disclaimer page emphasizes the parameters that were set when the calculator was developed. This is a new method of prediction and further data will need to be collected to establish its reliability ( et al., 2006). The prostate risk calculator is available online at http://www. compass.fhcrc.org/edrnnci/bin/calculator/main.asp. It should be noted that both the PSA value and DRE determination are variables that this calculator requires for evaluation. Men will need to continue their annual blood test and visit to the doctor's office for examination to use this calculation.

The future for prostate cancer screening, diagnosis, and treatment may well be guided by two large ongoing evidence-based trials. The National Cancer Institute is conducting a study to determine whether certain cancer screening tests will reduce death from cancer (NCI, 2006b). The European Randomized Study of Screening for Prostate Cancer is a large trial in seven countries in which the investigators are following 215,000 men. Both of these randomized trials will evaluate the screening of prostate cancer, quality of life factors, cost effectiveness, and specific mortality associated with prostate cancer (Han et al., 2004).

Men should be counseled about the risks and benefits of screening. They should be told that the PSA test has a margin of error that can cause undue worry and subsequent treatment. Providers should assess all factors for each individual when screening for prostate cancer. The man's age, race, family history, medications, life expectancy, and prostate size must all be evaluated. Family history should include a three-generation pedigree to assess the individual's risk (Wattendorf & Hadley, 2005). There is evidence to support an educated use of the PSA test and the available variables of the test. The bottom line is that PSA will continue to be used until there is a better biomarker to diagnose prostate cancer and differentiate between indolent and aggressive tumors.

Table 1. Age-Specific Reference Ranges for Serum PSA

Table 2. Recommendations for Screening

Table 3. Issues that Favor and Discourage PSA Screening

References

Albertsen, P.C., Hanley, J.A., & Fine, J. (2005). 20-year outcomes following conservative management of clinically localized prostate cancer. Journal of the American Medical Association, 293, 2095-2101. American Cancer Society (ACS). (2007). Cancer facts and figures. Retrieved July 9, 2007, from http://www.cancer.org/docroot/STT/content/STT1xCancerFactsFigures2007.asp American Society of Clinical Oncology (ASCO). (2006). People living with cancer. Retrieved October 7, 2006, from http://www.plwc.org/portal/ site/PLWC American Urological Association (AUA). (2000). Prostate-specific antigen (PSA): Best practice policy. Oncology, 14, 267-286. Arcangeli, C., Ornstein, D., Keetch, D., & Andriole, G. (1997) Prostate-specific antigen: The best prostatic tumor marker. Urologic Clinics of North America, 24, 299-305. Bill-Axelson, A., Holmberg, L., Ruutu, M., Haggman, M., Andersson, S., Bratell, S., et al. (2005). Radical prostatectomy versus watchful waiting in early prostate cancer. The New England Journal of Medicine, 352, 1977-1984. Brawer, M. (1999). Prostate-specific antigen: Current status. A Cancer Journal for Clinicians, 49, 264-281. , H.B., Pearson, J.D., Metter, E.J., Brant, L.J., Chan, D.W., Andres, R., et al. (1992). Longitudinal evaluation of prostate-specific antigen levels in men with and without prostate disease. Journal of the American Medical Association, 267, 2215-2220. , H.B., Ferrucci, L., Kettermann, A., Landis, P., , E., Epstein, J., et al. (2006). Detection of life-threatening prostate cancer with prostate-specific antigen velocity during a window of curability. Journal of the National Cancer Institute, 98, 1521-1527. Catalona, W., Partin, A., Slawin, K., Brawer, M., Flanigan, R., Patel, A., et al. (1998). Use of the percentage of free prostate-specific antigen to enhance differentiation of prostate cancer from benign prostatic disease: A prospective multicenter clinical trial. Journal of the American Medical Association, 279, 1542-1547. Catalona, W., , D., & Ornstein, D. (1997). Prostate cancer detection in men with serum PSA concentration of 2.6 to 4.0 ng/mL and benign prostate examination: Enhancement of specificity with free PSA measurement. Journal of the American Medical Association, 277, 1452-1455. Catalona, W., , D., Ratliff, T., Dodds, K., Coplen, D., Yaun, J., et al. (1991). Measurement of prostate specific antigen in serum as a screening test for prostate cancer. New England Journal of Medicine, 324, 1156-1161. Centers for Disease Control and Prevention (CDC). (2006). Prostate cancer screening: A decision guide. Retrieved September 12, 2006, from http:// apps.nccd.cdc.gov/EmailForm Chan, E., Haynes, M., O'Donnell, F., Bachino, C., & Vernon, S., (2003). Cultural sensitivity and informed decision making about prostate cancer screening. Journal of Community Health, 28, 393-405. Cookson, M., & , J. (2000). PSA testing: To screen or not to screen (prostate specific antigen). Consul tant, 40, 678. Coley, C., Barry, M., Fleming, C., & Mulley, A. (1997). Early detection of prostate cancer: Part 1: Prior probability and effectiveness of tests. ls of Internal Medicine, 126, 394-406. Dana Farber Cancer Institute. (2006). Supportive care. Retrieved September 22, 2006, from http://www.dfci.harvard.edu/can/supportivecare/View.aspx?lang=en & audience=0 & doc=CDR0000062818 Denmark-Wahnefried, W., Strigo, T., Catoe, K., Conaway, M., Brunetti, MJ., Rimer, B., et al. (1995). Knowledge, beliefs, and prior screening behavior among blacks and whites reporting for prostate cancer screening. Urology, 46, 346-351. Durkan, G., Sheikh, N., , P., Hildreth, A., & Greene, G. (2002). Improving prostate cancer detection with an extended-core transrectal ultrasonography-guided prostate biopsy protocol. BJU International, 89, 33- 39. Haiman, C., LeMarchand, L., Yamamato, J., Stram, D., Sheng, X., Kolonel, L., et al. (2007). Common genetic risk factor for colorectal and prostate cancer. Nature Genetics, Advance Online Publication, 1-3. Retrieved July 25, 2007, from http:// mutex.gmu.edu:2061/ng/journal/vaop/ncurrent/pdf/ng2098.pdf Han, M., Gann, P., & Catalona, W. (2004). Prostate-specific antigen and screening for prostate cancer. The Medical Clinics of North America, 88, 245-265. , R., & Lohr, K. (2002). Screening for prostate cancer: An update of the evidence. Retrieved September 17, 2006, from http://www.ahcpr.gov/ clinic/uspstf/uspsprca.htm sen, N., , K., Estey, E., & Voaklander, D. (2007). Open versus laparoscopic radical prostatectomy: A prospective comparison of postoperative urinary incontinence rates. The Journal of Urology, 177, 615-619. Jayadevappa, R., Chhatre, S., Weiner, M., Bloom, B., & Malkowicz, S. (2005). Medical care cost of patients with prostate cancer. Urologic Oncology: Seminars and Original Investigations, 23, 155-162. Johansson, J., Andren, O., Andersson, S., Dickman, P., Holmberg, L., Magnuson, A., et al. (2004). Natural history of early, localized prostate cancer. Journal of the American Medical Association, 291, 2713-2719. Kramer, B.S., Brown, M.L., Prorok, P.C., Potosky, A.L., & Gohagan, J.K. (1993). Prostate cancer screening: What we know and what we need to know. ls of Internal Medicine, 119(9), 914-923. Loeb, S., Roehl, K., Antenor, J., Catalona, W., Suarez, B., & Nadler R. (2006). Baseline prostate-specific antigen compared with median prostate-specific antigen for age group as a predictor of prostate cancer risk in men younger than 60 years old. Urology, 67, 316-320. Max, W., Rice, D., Sung, H., Michel, M., Breuer, W., & Zhang, X., (2002). The economic burden of prostate cancer, California, 1998. Cancer, 94, 2906-2913. Merenstein, D. (2004). Winners and losers. Journal of the American Medical Association, 291, 15-16. Moul, J.W. (2003). Population screening for prostate cancer and emerging concepts for young men. Clinics in Prostate Cancer, 2, 87-97. National Cancer Institute (NCI). (2006a). The prostate-specific antigen (PSA) test: Questions and answers. Retrieved September 6, 2006, from http://www.cancer.gov/cancertopics/factsheet/Detection/PSA National Cancer Institute (NCI). (2006b). Prostate cancer research results from the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial: Fact sheet. Retrieved September 9, 2006, from http:// www.cancer.gov/newscenter/pressreleases/PLCOProstateFactSheet National Cancer Institute (NCI). (2006c). Anxiety disorder. Retrieved Sep tem ber 22, 2006, from http://www.cancer. gov/cancertopics/pdq/supportive care/anxiety/HealthProfessional National Cancer Institute (NCI). (2007). SEER fact sheet. Retrieved July 11, 2007, from http://seer.cancer.gov/statfacts/html/prost.html National Institutes of Health (NIH). (2006). Prostate cancer genetic backgrounder. Retrieved October 2, 2006, from http://www.genome.gov/10003513 , C. (2004). Active surveillance towards a new paradigm in the management of early prostate cancer. The Lancet Oncology, 5, 101-106. , T., & Oesterling, J. (1997). Age-specific reference ranges for serum prostate-specific antigen. Urology Clinics of North America, 24, 339-351. Ruchlin, H., & Pellissier, J., (2001). An economic overview of prostate cancer. Cancer, 92, 2796-2810. Schroder, F. (2005). Detection of prostate cancer: The impact of the European randomized study of screening for prostate cancer (ERSPC). The Canadian Journal of Urology, 12(Suppl.), 2-6. Shaid, D.J. (2004). The complex etiology or prostate cancer. Human Molecular Genetics, 13(1), R103-R121. Sheridan, S., , R., & Woolf, S. (2004). Shared decision making about screening and chemoprevention. A suggested approach from the U.S. Preventative Services Task Force. Retrieved July 18, 2007, from http://www.ahrq.gov/clinic/3rduspstf/shared/sharedba.pdf Sirovich, B.E., Schwartz, L.M., & Woloshin, S. (2003). Screening men for prostate and colorectal cancer in the United States: Does practice reflect the evidence? Journal of the American Medical Association, 289, 1414-1420. Tanagho, E.A., & McAninch, J.W. (Eds.). (2004). 's general urology. Norwalk, CT: Appleton & Lange. , I., er, D., Goodman, P., Tangen, C., , L., Parnes, H., et al. (2004). Prevalence of prostate cancer among men with a prostate-specific antigen level less than/equal 4.0ng/mL. The New England Journal of Medicine, 350, 2239-2246. , I., Ankerst, D., Chi, C., Lucia, M., Goodman, P., Crowley, J., et al. (2005). Operation characteristics of prostate-specific antigen in men with an initial PSA level of 3.0ng/mL or lower. Journal of the American Medical Association, 294, 66-70. , I., Bermejo, C., , J., Basler, J., & Canby-Hagino, E. (2005). Screening for prostate cancer: Opportunities and challenges. Surgical Oncology Clinics of North America, 14, 747-760. , I., Ankerst, D., Chi, C., Goodman, P., Tangen, C., Lucia, M., et al. (2006). Assessing prostate cancer risk: Results from the prostate cancer prevention trial. Journal of the National Cancer Institute, 98, 529- 34. U.S. Department of Health and Human Services (USDHHS). (2003). National healthcare disparities report. Retrieved October 7, 2006, from http://www.qualitytools.ahrq.gov/disparitiesreport Walter, L., Berterthal, D., Lindquist, K., & Konety, B. (2006). PSA screening among elderly men with limited life expectancies. Journal of the American Medical Association, 296, 2336-2342. Wattendorf, D.J., & Hadley, D.W. (2005). Family history: The three-generation pedigree. American Family Physi cian, 72, 441-448. , S., & Crawford, E., (2004). Screening for prostate cancer: Current recommendations. Urologic Clinics of North America, 31, 219-226. Yeager, M., Orr, N., , R.B., s, K.B., Kraft, P., Wacholder, S., et al. (2007). Genome-wide association study of prostate cancer identifies a second risk locus at 8q24. Nature Genetics, 19(5), 645-649.

Morse Linn, BSN, CURN, is a Graduate Student, Adult Practice Program, Mason University, Fairfax, VA. She is a member of the Certification Board for Urologic Nurses and Associates (CBUNA). A. Ball, MD, BA, FACS, is an Attending Uro-Oncological Surgeon, INOVA Fairfax Hospital Cancer Center, INOVA Fairfax Campus, Virginia Commonwealth University Medical College, Fairfax, VA, and a Clinical Professor of Urology, Washington University Medical Center, Washington, DC.Ann Maradiegue, PhD, C-FNP, RN, is an Assistant Professor, Mason University School of Nursing, the College of Health and Human Services, Fairfax, VA.

Disclosure: The authors reported no actual or potential conflict of interest in relation to this continuing nursing education article.Urologic Nursing Editorial Board Statements of Disclosure: Bradway, PhD, RN, disclosed that she is on the Consulting Board for Boehringer Ingelheim Pharmaceuticals, Inc.Kaye K. Gaines, MS, ARNP, CUNP, disclosed that she is on the Speakers´ Bureau for Pfizer, Inc., and Novartis Oncology.Sally S. , MN, CMSRN, disclosed that she is on the Advisory Board for Roche/Abbott Labs.All other Urologic Nursing Editorial Board members reported no actual or potential conflict of interest in relation to this continuing nursing education article.

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