Clinical Policy Bulletin: Prostate Cancer Screening
Aetna considers prostate-specific antigen (PSA) screening a medically necessary preventive service for men aged 40 years and older, and for men under 40 years of age who are at high-risk for prostate cancer. Risk groups include African-American men and men with a family history of prostate cancer.
When used for routine screening, annual PSA screening is considered medically necessary, but additional PSA tests may be considered medically necessary in men with previously elevated PSAs or signs or symptoms of disease.
Aetna considers diagnostic PSA testing medically necessary for men of all ages with signs or symptoms of prostate cancer, and for follow-up of men with prostate cancer.
Aetna considers annual digital rectal examination (DRE) a medically necessary preventive service.
Aetna considers alpha-methylacyl coenzyme A racemase (AMACR), early prostate cancer antigen, endoglin, E twenty-six (ETS) gene fusions, human kallikrein 2, interleukin-6, prostate cancer gene 3 (PCA3), and transforming growth factor-beta 1 experimental and investigational for prostate cancer screening because they have no proven value for this indication.
Aetna considers measurement of selenium in the blood or in tissues (such as toenail clippings) experimental and investigational to assess the risk of developing prostate cancer because it has no proven value for this indication.
Aetna considers the analysis of prostatic fluid electrolyte composition (e.g., citrate, zinc; not an all inclusive list) experimental and investigational for prostate cancer screening because it has no proven value for this indication.
Note: Some plans exclude coverage of preventive services. Please check benefit plan descriptions for details. Medically necessary diagnostic PSA testing is covered regardless of whether the member has preventive service benefits.
The decision to perform routine prostate cancer screening with digital rectal examination (DRE) or prostate-specific antigen (PSA) is left to the discretion of the clinician. Patients who request screening should be given objective information about the potential benefits and harms of early detection and treatment.
The American Cancer Society (ACS) recommends PSA screening for all men over age 50 and at age 45 for men at higher risk (e.g., men with a family history of prostate cancer and African-American men). Similar recommendations have been issued by the American Urological Association (AUA) and the American College of Radiology. The ACS, however, acknowledges that currently there is no clinical trial evidence that screening for prostate cancer is associated with a reduction in mortality.
The updated ACS guideline for the early detection of prostate cancer (Wolf et al, 2010) recommends both the PSA blood test and DRE should be offered annually, beginning at age 50, to men who have at least a 10-year life expectancy. Men at high-risk (African-American men and men with a strong family of 1 or more first-degree relatives (father, brothers) diagnosed at an early age) should begin testing at age 45. Men at even higher risk, due to multiple first-degree relatives affected at an early age, could begin testing at age 40. Depending on the results of this initial test, no further testing might be needed until age 45. The ACS states that information should be provided to all men about what is known and what is uncertain about the benefits and limitations of early detection and treatment of prostate cancer so that they can make an informed decision about testing. Men who ask their doctor to make the decision on their behalf should be tested. The ACS states that discouraging testing is inappropriate. Furthermore, not offering testing is also inappropriate.
In a review on prostate cancer screening, Ilic and colleagues (2011) concluded that prostate cancer screening did not significantly decrease all-cause or prostate cancer-specific mortality in a combined meta-analysis of 5 randomized controlled trials. Any benefits from prostate cancer screening may take greater than 10 years to accrue; therefore, men who have a life expectancy of less than 10 to 15 years should be informed that screening for prostate cancer is not beneficial and has harms.
The AUA recommends that prostate cancer screening be offered to men over age 50, and at age 40 for men at high-risk, with the physician explaining the uncertain benefits and risks of such screening.
The National Comprehensive Cancer Network (2005) recommends baseline screening beginning at age 40, especially for men in high-risk groups. Risk groups include African-American men and men with a family history of prostate cancer.
Most professional societies do not recommend routine screening for prostate cancer with DRE or serum tumor markers (e.g., PSA). These include the American Academy of Family Physicians, the U.S. Preventive Services Task Force (USPSTF), the Institute for Clinical Systems Improvement, the Canadian Task Force on the Periodic Health Examination, the American College of Preventive Medicine, the U.S. Office of Technology Assessment, the American Society for Internal Medicine and American College of Physicians, the National Cancer Institute, the Centers for Disease Control and Prevention, and the technology assessment agencies of Canada, England, Sweden, and Australia.
The USPSTF evaluated randomized, controlled trials of the benefits of prostate cancer screening, cohort and cross-sectional studies of the psychological harms of false-positive PSA test results, and evidence on the natural history of PSA-detected prostate cancer and concluded that in men younger than age 75 years, the current evidence is insufficient to determine whether treatment for prostate cancer detected by screening improves health outcomes compared with treatment after clinical detection. In men aged 75 years or older, the USPSTF found no direct evidence of benefits of prostate cancer screening and recommends against screening for prostate cancer in men aged 75 years or older.
If screening is to be performed, the generally accepted approach is to screen with DRE and PSA and to limit screening to men with a life expectancy of greater than 10 years. There is currently insufficient evidence to determine the need and optimal interval for repeat screening or whether PSA thresholds must be adjusted for density, velocity, or age.
Schenk-Braat and Bangma (2006) noted that PSA is currently the most important biochemical marker for the diagnosis of prostate cancer. Because of the limited specificity of PSA, clinically irrelevant tumors and benign abnormalities are also detected that can potentially lead to over-treatment and the associated physical as well as emotional burden for the patient. Furthermore, PSA is used as an indicator of progression or clinical response following prostate cancer therapy, but the prognostic value of this marker is limited. Ongoing research is examining several alternative markers (e.g., osteoprotegerin, human kallikrein 2, and the gene DD3(PCA3)) that may improve the specificity of current PSA-based diagnostics and the prognostic value of PSA.
Prostate-specific antigen velocity, the yearly rate of increase of PSA, has not been proven to improve the test characteristics of PSA, Schroder and colleagues (2006) stated that PSA-driven screening has been applied to a large part of the male population in many countries. An elevated PSA in secondary screens may indicate benign enlargement of the prostate rather than prostate cancer. In such cases the yearly rate of increase of PSA (PSA velocity [PSAV]) may improve the test characteristics of PSA. These investigators examined if PSAV predict prostate cancer in pre-screened populations. Data from the European Randomized Study of Screening for Prostate Cancer Rotterdam were used to study the issue. Relative sensitivity, relative specificity, and positive predictive value (PPV) were calculated. Logistic regression analysis was used to compare odds ratios for positive biopsies. The relationship between PSAV and parameters of tumor aggressiveness was investigated. A total of 588 consecutive participants were identified who presented at their first screening with PSA values less than 4.0 and who progressed to PSA values greater than 4.0 ng/ml 4 years later were included in this study. None was biopsied in round-1, all were biopsied in round-2. Relative sensitivity and specificity depend strongly on PSAV cut-offs of 0.25 to 1.0 ng/ml/year. The use of PSAV cut-offs did not improve the PPV of the PSA cut-off of 4.0 ng/ml, nor did any of the PSAV cut-offs improve the odds ratio (OR) for identifying prostate cancer with respect to the cut-off value of 4.0 ng/ml. The rate of aggressive cancers seems to increase with increasing PSAV. The authors concluded that PSAV did not improve the detection characteristics of a PSA cut-off of 4.0 ng/ml in secondary screening after 4 years.
Wolters et al (2009) evaluated the value of PSAV in screening for prostate cancer. Specifically, the role of PSAV in lowering the number of unnecessary biopsies and reducing the detection rate of indolent prostate cancer was evaluated. All men included in the study cohort were subjects in the European Randomized Study of Screening for Prostate Cancer (ERSPC), Rotterdam section. During the first and second screening round, a PSA test was performed on 2,217 men, and all underwent a biopsy during the second screening round 4 years later. Prostate specific antigen velocity was calculated and biopsy outcome was classified as benign, possibly indolent prostate cancer, or clinically significant prostate cancer. A total of 441 cases of prostate cancer were detected, 333 were classified as clinically significant and 108 as possibly indolent. The use of PSAV cut-offs reduced the number of biopsies but led to important numbers of missed (indolent and significant) prostate cancer; PSAV was predictive for prostate ancer (OR: 1.28, p < 0.001) and specifically for significant prostate cancer (OR: 1.46, p < 0.001) in uni-variate analyses. However, multi-variate analyses using age, PSA, prostate volume, DRE and transrectal ultrasonography outcome, and previous biopsy (yes/no) showed that PSAV was not an independent predictor of prostate cancer (OR: 1.01, p = 0.91) or significant prostate cancer (OR: 0.87, p = 0.30). The authors concluded that the use of PSAV as a biopsy indicator would miss a large number of clinically significant cases of prostate cancer with increasing PSAV cut-offs. In this study, PSAV was not an independent predictor of a positive biopsy in general or significant prostate cancer on biopsy. Thus, PSAV does not improve the ERSPC screening algorithm.
The role of selenium in cancer prevention has been the subject of recent study and debate. Population studies suggest that people with cancer are more likely to have low selenium levels (measured in the blood or in tissues such as toenail clippings) than healthy matched individuals. However, in most cases it is not clear if low selenium levels are a cause or merely a consequence of disease. Initial evidence from the Nutritional Prevention of Cancer (NPC) trial suggests that selenium supplementation reduces the risk of prostate cancer among men with normal baseline PSA levels and low selenium blood levels. The ongoing Selenium and Vitamin E Cancer Prevention Trial (SELECT) aims to definitively address the role of selenium in prostate cancer prevention. The study, which spans from 2001 to 2013, will include 32,400 men. Currently, it is unclear if selenium is beneficial in the treatment of prostate cancer or any type of cancer. Measurement of body selenium (e.g., in serum, toenail clippings) has no proven value in the prevention of prostate cancer.
Costello and Franklin (2009) proposed that changes in prostatic fluid composition could provide accurate and reliable biomarkers for the screening of prostate cancer. Most notable is the consistent and significant decrease in citrate and zinc that is associated with the development and progression of prostate cancer. These researchers provided the clinical and physiological basis and the evidence in support of the utility of prostatic fluid analysis as an effective approach for screening/detection of prostate cancer, especially early stage and "at-risk" subjects. The problem of interference from benign prostatic hypertrophy that hampers PSA testing is eliminated in the potential prostatic fluid biomarkers. The potential development of rapid, simple, direct, accurate clinical tests would provide additional advantageous conditions. The authors stated that further exploration and development of citrate, zinc and other electrolytes as prostatic fluid biomarkers are needed to address this critical prostate cancer issue.
A long-term randomized controlled clinical trial found prostate cancer screening had no effect on mortality (Andriole et al, 2009). From 1993 through 2001, investigators randomly assigned 76,693 men at 10 U.S. study centers to receive either annual screening (38,343 subjects) or usual care as the control (38,350 subjects). Men in the screening group were offered annual PSA testing for 6 years and DRE for 4 years. The subjects and health care providers received the results and decided on the type of follow-up evaluation. Usual care sometimes included screening, as some organizations have recommended. The numbers of all cancers and deaths and causes of death were ascertained. In the screening group, rates of compliance were 85 % for PSA testing and 86 % for DRE. Rates of screening in the control group increased from 40 % in the first year to 52 % in the sixth year for PSA testing and ranged from 41 to 46 % for DRE. After 7 years of follow-up, the incidence of prostate cancer per 10,000 person-years was 116 (2,820 cancers) in the screening group and 95 (2,322 cancers) in the control group (rate ratio, 1.22; 95 % confidence interval [CI]: 1.16 to 1.29). The incidence of death per 10,000 person-years was 2.0 (50 deaths) in the screening group and 1.7 (44 deaths) in the control group (rate ratio, 1.13; 95 % CI: 0.75 to 1.70). The data at 10 years were 67 % complete and consistent with these overall findings. An important limitation of this study is that subjects in the control group underwent considerable screening outside of the clinical trial. An accompanying editorial (Barry, 2009) commented that serial PSA screening has at best a modest effect on prostate cancer mortality during the first decade of follow-up, and that this benefit comes at the cost of substantial over-diagnosis and over-treatment.
Available evidence shows that the majority of men with low-risk prostate tumors receive aggressive treatment, despite the risk of complications. Shao and colleagues (2010) used the Surveillance, Epidemiology and End Results (SEER) database to study the records of 123,934 men over the age of 25 who had newly diagnosed prostate cancer from 2004 to 2006. About 14 % of the men had PSA values lower than 4, generally younger men. In that group, 54 % had low-risk disease that could be safely monitored for progression with little risk. Nonetheless, 75 % of them received aggressive treatment, including a radical prostatectomy and radiation therapy. Among men in that group over the age of 65, in which "watchful waiting" is generally advised for low-risk disease, 66 % had aggressive therapy. In both cases, the percentages were similar to those in the group with PSA levels between 4 and 20.
Mazzola et al (2011) stated that the introduction and widespread adoption of PSA has revolutionized the way prostate cancer is diagnosed and treated. However, the use of PSA has also led to over-diagnosis and over-treatment of prostate cancer resulting in controversy about its use for screening. Prostate specific antigen also has limited predictive accuracy for predicting outcomes after treatment and for making clinical decisions about adjuvant and salvage therapies. Thus, there is an urgent need for novel biomarkers to supplement PSA for detection and management of prostate cancer. A plethora of promising blood- and urine-based biomarkers have shown promise in early studies and are at various stages of development (human kallikrein 2, early prostate cancer antigen, transforming growth factor-beta 1, interleukin-6, endoglin, prostate cancer gene 3 (PCA3), alpha-methylacyl coenzyme A racemase (AMACR) and E twenty-six (ETS) gene fusions).
CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
CPT codes not covered for indications listed in the CPB:
Other CPT codes related to the CPB:
HCPCS codes covered if selection criteria are met:
Prostate cancer screening; digital rectal examination
Prostate cancer screening; prostate specific antigen test (PSA)
HCPCS codes not covered for indications listed in the CPB:
Prostate cancer antigen 3 (PCA3) testing
ICD-9 codes covered if selection criteria are met:
Malignant neoplasm of prostate
Benign neoplasm of prostate
Carcinoma in situ of prostate
Neoplasm of uncertain behavior of prostate
600.00 - 600.91
Hypertrophy of prostate
Dysplasia of prostate
Elevated prostate specific antigen (PSA)
Personal history of malignant neoplasm of prostate
Family history of malignant neoplasm of prostate
Special screening for malignant neoplasm of prostate
Genetic susceptibility to malignant neoplasm of prostate
Other ICD-9 codes related to the CPB:
788.20 - 788.29
Retention of urine
788.41 - 788.43
Frequency of urination and polyuria
788.61 - 788.65
Other abnormality of urination
The above policy is based on the following references:
U.S. Preventive Services Task Force. Screening for prostate cancer: Recommendations and rationale. Ann Intern Med. 2002;137(11):915-916.
American College of Radiology (ACR). Resolution No. 36. Reston, VA: ACR; October 1991.
Canadian Task Force on the Periodic Health Examination. Canadian Guide to Clinical Preventive Health Care. Ottawa, ON: Canada Communications Group; 1994.
U.S. Congress, Office of Technology Assessment (OTA). Costs and effectiveness of prostate cancer screening in elderly men. Pub. No. OTA-PB-H-145. Washington, DC: U.S. Government Printing Office; 1995.
Coley CM, Barry MJ, Fleming C, et al. Early detection of prostate cancer. Part I: Prior probability and effectiveness of tests. Ann Intern Med. 1997;126(5):394-406.
Coley CM, Barry MJ, Fleming C, et al. Early detection of prostate cancer. Part II: Estimating the risks, benefits, and costs. American College of Physicians. Ann Intern Med. 1997;126(6):468-469.
Middleton RG. Prostate cancer: Are we screening and treating too much? Ann Intern Med. 1997;126(6):465-467.
Ferrini R, Woolf SH. Screening for prostate cancer in American men. American College of Preventive Medicine Practice Policy Statement. Am J Prev Med. 1998;15(1):81-84.
von Eschenbach A, Ho R, Murphy GP, et al. American Cancer Society guideline for early detection of prostate cancer: Update 1997. CA Cancer J Clin. 1997;47(5):261-264.
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American Academy of Family Physicians. Summary of policy recommendations for periodic health examinations. Leawood, KS: American Academy of Family Physicians; August 2003.
Institute for Clinical Systems Improvement (ICSI). Preventive services for adults. ICSI Health Care Guidelines. Bloomington, MN: ICSI; September 2004.
Peters S, Jovell AJ, Garcia-Altes A, Serra-Prat M. Screening and clinical management of prostate cancer: A cross-national comparison. Int J Technol Assess Health Care. 2001;17:215-221.
Harris R, Lohr KN. Screening for prostate cancer: An update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2002;137(11):917-929.
Brawer MK. Clinical usefulness of assays for complexed prostate-specific antigen. Urol Clin North Am. 2002;29(1):193-203, xi.
Small EJ, Roach M 3rd. Prostate-specific antigen in prostate cancer: A case study in the development of a tumor marker to monitor recurrence and assess response. Semin Onco. 2002;29(3):264-273.
Slaughter PM, Pinfold SP, Laupacis A. Prostate-specific antigen (PSA) screening in asymptomatic men. Toronto, ON: Institute for Clinical Evaluative Sciences (ICES); 2002.
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Denmeade SR, Isaacs JT. The role of prostate-specific antigen in the clinical evaluation of prostatic disease. BJU Int. 2004;93 Suppl 1:10-15.
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American Cancer Society (ACS). Recommendations from the American Cancer Society Workshop on Early Prostate Cancer Detection, May 4-6, 2000 and ACS guideline on testing for early prostate cancer detection: Update 2001. CA Cancer J Clin. 2001;51(1):39-44.
Smith RA, Cokkinides V, Eyre HJ. American Cancer Society guidelines for the early detection of cancer, 2003. CA Cancer J Clin. 2003;53(1):27-43.
American Urological Association. Prostate-specific antigen (PSA) best practice policy. Oncology. 2000;14(2):267-286.
Carroll P, Coley C, McLeod D, et al. Prostate-specific antigen best practice policy--part I: Early detection and diagnosis of prostate cancer. Urology. 2001;57(2):217-224.
Carroll P, Coley C, McLeod D, et al. Prostate-specific antigen best practice policy--part II: Prostate cancer staging and post-treatment follow-up. Urology. 2001;57(2):225-229.
University of Michigan Health System. Adult preventive health care: Cancer screening. Ann Arbor, MI: University of Michigan Health System; May 2004.
Medical Services Advisory Committee (MSAC). Prostate specific antigen (PSA) near patient testing for diagnosis and management of prostate cancer. MSAC Application 1068. Canberra, ACT: MSAC; 2005.
Ilic D, O'Connor D, Green S, Wilt T. Screening for prostate cancer. Cochrane Database Syst Rev. 2006:(3):CD004720.
Mambourg F, Van den Bruel A, Devriese S, et al. Health technology assessment: The use of prostate specific antigen (PSA) in prostate cancer screening. KCE Reports Vol. 31B. Brussels, Belguim: Belgian Health Care Knowledge Centre (KCE); 2006.
Schenk-Braat EA, Bangma CH. The search for better markers for prostate cancer than prostate-specific antigen. Ned Tijdschr Geneeskd. 2006;150(23):1286-1290.
Ilic D, O'Connor D, Green S, Wilt T. Screening for prostate cancer: A Cochrane systematic review. Cancer Causes Control. 2007;18(3):279-285.
Bryant RJ, Hamdy FC. Screening for prostate cancer: An update. Eur Urol. 2008;53(1):37-44.
Lim LS, Sherin K; ACPM Prevention Practice Committee. Screening for prostate cancer in U.S. men ACPM position statement on preventive practice. Am J Prev Med. 2008;34(2):164-170.
Lin K, Lipsitz R, Miller T, Janakiraman S. Benefits and harms of prostate-specific cancer screening: An evidence update for the U.S. Preventive Services Task Force. Evidence Synthesis No. 63. Rockville, MD: Agency for Healthcare Research and Quality (AHRQ); 2008.
U.S. Preventive Services Task Force. Screening for prostate cancer: U.S. Preventive Services Task Force Recommendation Statement. Ann Intern Med. 2008;149:185-191.
Satia JA, King IB, Morris JS, Stratton K, White E. Toenail and plasma levels as biomarkers of selenium exposure. Ann Epidemiol. 2006;16(1):53-58.
van den Brandt PA, Zeegers MP, Bode P, Goldbohmm A. Toenail selenium levels and the subsequent risk of prostate cancer: A prospective Cohort study. Cancer Epidemiology, Biomarkers & Prevention. 2003;12:866-871. Available at: http://cebp.aacrjournals.org/cgi/reprint/12/9/866.pdf. Accessed August 14, 2008.
Reid ME, Duffield-Lillico AJ, Slate E, et al. The nutritional prevention of cancer: 400 mcg per day selenium treatment. Nutr Cancer. 2008;60(2):155-163.
Costello LC, Franklin RB. Prostatic fluid electrolyte composition for the screening of prostate cancer: A potential solution to a major problem. Prostate Cancer Prostatic Dis. 2009;12(1):17-24.
Schröder FH, Roobol MJ, van der Kwast TH, et al. Does PSA velocity predict prostate cancer in pre-screened populations? Eur Urol. 2006;49(3):460-465; discussion 465.
Wolters T, Roobol MJ, Bangma CH, Schröder FH. Is prostate-specific antigen velocity selective for clinically significant prostate cancer in screening? European Randomized Study of Screening for Prostate Cancer (Rotterdam). Eur Urol. 2009;55(2):385-392.
Schröder FH, Hugosson J, Roobol MJ, et al; ERSPC Investigators. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med. 2009;360(13):1320-1328.
Shao YH, Albertsen PC, Roberts CB, et al. Risk profiles and treatment patterns among men diagnosed as having prostate cancer and a prostate-specific antigen level below 4.0 ng/mL. Arch Intern Med. 2010;170(14):1256-1261.
Lu-Yao GL, Albertsen PC, Moore DF, et al. Outcomes of localized prostate cancer following conservative management. JAMA. 2009;302(11):1202-1209.
Shappley WV 3rd, Kenfield SA, Kasperzyk JL, et al. Prospective study of determinants and outcomes of deferred treatment or watchful waiting among men with prostate cancer in a nationwide cohort. J Clin Oncol. 2009;27(30):4980-4985.
Zietman A. Evidence-based medicine, conscience-based medicine, and the management of low-risk prostate cancer. J Clin Oncol. 2009;27(30):4935-4936.
Esserman L, Shieh Y, Thompson I. Rethinking screening for breast cancer and prostate cancer. JAMA. 2009;302(15):1685-1692.
Andriole GL, Crawford ED, Grubb RL 3rd, et al; PLCO Project Team. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med. 2009;360(13):1310-1319.
Barry MJ. Screening for prostate cancer -- the controversy that refuses to die. N Engl J Med. 2009;360(13):1351-1354.
Greene KL, Albertsen PC, Babaian RJ, et al. Prostate specific antigen best practice statement: 2009 update. J Urol. 2009;182(5):2232-2241.
Shao YH, Albertsen PC, Roberts CB, et al. Risk profiles and treatment patterns among men diagnosed as having prostate cancer and a prostate-specific antigen level below 4.0 ng/ml. Arch Intern Med. 2010;170(14):1256-1261.
Wolf AM, Wender RC, Etzioni RB, et al; American Cancer Society Prostate Cancer Advisory Committee. American Cancer Society guideline for the early detection of prostate cancer: Update 2010. CA Cancer J Clin. 2010;60(2):70-98.
Mazzola CR, Ghoneim T, Shariat SF. Emerging biomarkers for the diagnosis, staging and prognosis of prostate cancer. Prog Urol. 2011;21(1):1-10.
Ilic D, O'Connor D, Green S, Wilt TJ. Screening for prostate cancer: An updated Cochrane systematic review. BJU Int. 2011;107(6):882-891.
Djulbegovic M, Beyth RJ, Neuberger MM, et al. Screening for prostate cancer: Systematic review and meta-analysis of randomised controlled trials. BMJ. 2010;341:c4543.
Chou R, Croswell JM, Dana T, et al. Screening for prostate cancer: A review of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2011;155(11):762-771.
National Comprehensive Cancer Network (NCCN). Prostate cancer early detection. NCCN Clinical Practice Guidelines in Oncology version 2.2012. Fort Washington, PA: NCCN; 2012.
Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.