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Prostate Cancer Screening (PDQ®)


Incidence and Mortality

Prostate cancer is the most common cancer diagnosed in North American men, excluding skin cancers. It is estimated that in 2015, approximately 220,800 new cases and 27,540 prostate cancer-related deaths will occur in the United States.[1] Prostate cancer is now the second leading cause of cancer death in men, exceeded only by lung cancer. It accounts for 26% of all male cancers and 9% of male cancer-related deaths.[1] Age-adjusted incidence rates increased steadily over the past several decades, with particularly dramatic increases associated with the inception of widespread use of prostate-specific antigen (PSA) screening in the late 1980s and early 1990s, followed by a more recent fall in incidence. Between 2007 and 2011, mortality rates decreased by 3.2% per year.[1] It has been suggested that declines in mortality rates in certain jurisdictions reflect the benefit of PSA screening,[2] but others have noted that these observations may be explained by independent phenomena such as improved treatment effects.

Regional differences have been observed in prostate cancer incidence and mortality rates and in rates of radical prostatectomy. Until 1989, the increased incidence was most likely the result of increased tumor detection due to increasing rates of transurethral prostatectomy.[3,4] Subsequent increases were most likely the result of widespread use of PSA testing for early detection and screening.[5,6] Variable incidence rates may reflect variability in the intensity of early detection practices across the United States and other jurisdictions. While differences in aggregate mortality by regions of the United States have not been observed, considerable variation in mortality rates between African American and white men are seen.[7,8] (Refer to the Population Observations on Early Detection, Incidence, and Prostate Cancer Mortality section of this summary for more information.)

Risk Factors

Prostate cancer is uncommonly seen in men younger than 50 years; the incidence rises rapidly with each decade thereafter. The incidence rate is higher in African American men than in white men. From 2005 to 2009, the overall age-adjusted incidence rate was 236 per 100,000 for African American men and 146.9 per 100,000 for white men.[9] African American males have a higher mortality from prostate cancer, even after attempts to adjust for access-to-care factors.[10] Men with a family history of prostate cancer are at an increased risk of the disease compared with men without this history.[11,12] Other potential risk factors besides age, race, and family history of prostate cancer include alcohol consumption, vitamin or mineral interactions, and other dietary habits.[13-17] A significant body of evidence suggests that a diet high in fat, especially saturated fats and fats of animal origin, is associated with a higher risk of prostate cancer.[18,19] Other possible dietary influences include selenium, vitamin E, vitamin D, lycopene, and isoflavones. (Refer to the PDQ summary on Prostate Cancer Prevention for more information.) Evidence from a nested case-control study within the Physicians’ Health Study,[20] in addition to a case-control study [21] and a retrospective review of screened prostate cancer patients,[22] suggests that higher plasma insulin-like growth factor-I levels may be associated with a higher prostate cancer risk.[23] Not all studies, however, have confirmed this association.[24] The estimated lifetime risk of diagnosis of prostate cancer is about 16.5%,[25] and the lifetime risk of dying from this disease is 2.8%.[26]

The biology and natural history of prostate cancer is not completely understood. Rigorous evaluation of any prostate cancer screening modality is desirable because the natural history of the disease is variable, and appropriate treatment is not clearly defined. Although the prevalence of prostate cancer and preneoplastic lesions found at autopsy steadily increases for each decade of age, most of these lesions remain clinically undetected.[27] An autopsy study of white and Asian men also found an increase in occult prostate cancer with age, reaching nearly 60% in men older than 80 years. More than 50% of cancers in Asian men and 25% of cancers in white men had a Gleason score of 7 or greater, suggesting that Gleason score may be an imprecise indicator of clinically insignificant prostate cancer.[28]

There is an association between primary tumor volume and local extent of disease, progression, and survival.[29] A review of a large number of prostate cancers in radical prostatectomy, cystectomy, and autopsy specimens showed that capsular penetration, seminal vesicle invasion, and lymph node metastases were usually found only with tumors larger than 1.4 cc.[30] Furthermore, the semiquantitative histopathologic grading scheme proposed by Gleason is reasonably reproducible among pathologists and correlates with the incidence of nodal metastases and with patient survival in a number of reported studies.[31]

Cancer statistics from the American Cancer Society and the National Cancer Institute indicated that between 2002 and 2008, the proportion of disease diagnosed at a locoregional stage and at a distant stage was 93% and 4% for whites, compared with 91% and 6% for African Americans, respectively.[9] Stage distribution of prostate cancer is affected substantially by the intensity of early detection efforts.

Pathologic stage does not always reflect clinical stage and upstaging (owing either to extracapsular extension, positive margins, seminal vesicle invasion, or lymph node involvement) occurs frequently. Of the prostate cancers detected by digital rectal exam (DRE) in the pre-PSA era, 67% to 88% were at a clinically localized stage (T1–2, NX, M0 [T = tumor size, N = lymph node involvement, and M = metastasis]).[32,33] However, in one of those series of 2,002 patients undergoing annual screening DRE, only one-third of men proved to have pathologically organ-confined disease.[33]

With the proliferation of PSA for early detection, reviews of large numbers of asymptomatic men with prostate cancer found that most have organ-confined disease. One study found that 63% of cancers detected in men undergoing their first screening PSA were pathologically organ-confined cancers; the percentage increased to 71% if cancer was detected on a subsequent examination.[34] In a series of 2,999 men undergoing screening with PSA, DRE, and transrectal ultrasound, 62% of the tumors detected were reported to be pathologically organ-confined.[35] While the proportion of node-positive cancers in the pre-PSA era were in the range of 25% for patients with ostensibly localized disease, current series report proportions as low as 3%.[36] Stage T1c tumors detected by serial PSA and removed by radical prostatectomy are organ-confined in 79% of cases.[37]

Survival rates for prostate cancer have improved from 1974 to the present. Lead-time and length-bias effects of early detection and the possible influence of stage migration must also be considered when trends in survival data are interpreted.[38] Reported survival rates may also vary, depending on whether the analytical methods reflect crude disease-specific rates (absolute disease-specific survival) or take into account competing risks for the given age group (relative disease-specific survival).


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  12. Matikainen MP, Schleutker J, Mörsky P, et al.: Detection of subclinical cancers by prostate-specific antigen screening in asymptomatic men from high-risk prostate cancer families. Clin Cancer Res 5 (6): 1275-9, 1999. [PUBMED Abstract]
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  14. Platz EA, Leitzmann MF, Rimm EB, et al.: Alcohol intake, drinking patterns, and risk of prostate cancer in a large prospective cohort study. Am J Epidemiol 159 (5): 444-53, 2004. [PUBMED Abstract]
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  17. Morton MS, Griffiths K, Blacklock N: The preventive role of diet in prostatic disease. Br J Urol 77 (4): 481-93, 1996. [PUBMED Abstract]
  18. Fleshner NE, Klotz LH: Diet, androgens, oxidative stress and prostate cancer susceptibility. Cancer Metastasis Rev 17 (4): 325-30, 1998-99. [PUBMED Abstract]
  19. Clinton SK, Giovannucci E: Diet, nutrition, and prostate cancer. Annu Rev Nutr 18: 413-40, 1998. [PUBMED Abstract]
  20. Chan JM, Stampfer MJ, Giovannucci E, et al.: Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 279 (5350): 563-6, 1998. [PUBMED Abstract]
  21. Oliver SE, Barrass B, Gunnell DJ, et al.: Serum insulin-like growth factor-I is positively associated with serum prostate-specific antigen in middle-aged men without evidence of prostate cancer. Cancer Epidemiol Biomarkers Prev 13 (1): 163-5, 2004. [PUBMED Abstract]
  22. Turkes A, Peeling WB, Griffiths K: Serum IGF-1 determination in relation to prostate cancer screening: possible differential diagnosis in relation to PSA assays. Prostate Cancer Prostatic Dis 3 (3): 173-175, 2000. [PUBMED Abstract]
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  28. Zlotta AR, Egawa S, Pushkar D, et al.: Prevalence of prostate cancer on autopsy: cross-sectional study on unscreened Caucasian and Asian men. J Natl Cancer Inst 105 (14): 1050-8, 2013. [PUBMED Abstract]
  29. Freedland SJ, Humphreys EB, Mangold LA, et al.: Risk of prostate cancer-specific mortality following biochemical recurrence after radical prostatectomy. JAMA 294 (4): 433-9, 2005. [PUBMED Abstract]
  30. McNeal JE, Bostwick DG, Kindrachuk RA, et al.: Patterns of progression in prostate cancer. Lancet 1 (8472): 60-3, 1986. [PUBMED Abstract]
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  • Updated: April 2, 2015