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Prostate Cancer Prevention (PDQ®)
Patient Version   Health Professional Version   Last Modified: 08/26/2008



Purpose of This PDQ Summary






Summary of Evidence






Significance






Risk Factors for Prostate Cancer Development






Opportunities for Prevention






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Significance

Incidence and Mortality



Incidence and Mortality

Carcinoma of the prostate is the most common tumor in men in the United States, with an estimated 186,320 new cases and 28,660 deaths expected in 2008.[1] A wide range of estimates of the impact of the disease are notable. The disease is histologically evident in as many as 34% of men in their fifth decade and in up to 70% of men aged 80 years and older.[2,3] Prostate cancer will be diagnosed in almost one fifth of U.S. men during their lifetime, yet only 3% of men will be expected to die of the disease.[4] The estimated reduction in life expectancy of men who die of prostate cancer is approximately 9 years.[5]

The extraordinarily high rate of clinically occult prostate cancer in the general population compared with the 20-fold lower likelihood of death from the disease indicates that many of these cancers have low biologic risk. Concordant with this observation are the many series of patients with prostate cancer managed by surveillance alone with relatively good survival rates at 5 and 10 years of follow-up.[6] Data demonstrate, however, that with prolonged 10-year follow-up of moderately differentiated (which constitute the majority of tumors detected [7]) and poorly differentiated tumors, there is a substantial risk of disease progression and death from prostate cancer.[8]

Because of marked variability in tumor differentiation from one microscopic field to another, many pathologists will report the range of differentiation among the malignant cells that are present in a biopsy using the Gleason grading system. This grading system includes five histologic patterns distinguished by the glandular architecture of the cancer. The architectural patterns are identified and assigned a grade from 1 to 5 with 1 being the most differentiated and 5 being the least differentiated. The sum of the grades of the predominant and next most prevalent will range from 2 (well-differentiated tumors) to 10 (undifferentiated tumors).[9,10] Systematic changes to the histological interpretation of biopsy specimens by anatomical pathologists have occurred during the prostate-specific antigen (PSA) screening era (i.e., since about 1985) in the United States.[11] This phenomenon, sometimes called “grade inflation,” is the apparent increase in the distribution of high-grade tumors in the population over time but in the absence of a true biological or clinical change. It is possibly the result of an increasing tendency for pathologists to read tumor grade as more aggressive, resulting in a higher preponderance to treat these cancers aggressively.[12]

Treatment options available for prostate cancer include radical prostatectomy, external-beam radiation therapy, brachytherapy, cryotherapy, androgen deprivation with luteinizing hormone-releasing hormone analogs and/or antiandrogens, intermittent androgen deprivation, cytotoxic agents, and surveillance. Of all the means of management, only radical prostatectomy has been found to be superior to surveillance in men with localized prostate cancer in terms of reduced rates of metastases (relative hazard = 0.63; 95% CI, 0.41–0.96) and disease specific (relative hazard = 0.5; 95% CI, 0.27–0.91) and overall mortalities.[13] However, the relative efficacy of radical prostatectomy to the other forms of treatment has not been adequately addressed.[14] Confounding issues in the treatment of prostate cancer include side effects with treatment, inability to predict the natural history of a given cancer, patient comorbidity that may affect an individual’s likelihood of surviving long enough to be at risk for disease morbidity and mortality, and an increasing body of evidence suggesting that careful PSA monitoring following treatment may indicate a substantial fraction of treatment failures.[15]

Because of considerable uncertainty regarding the efficacy of treatment and the difficulty with selecting patients for whom there is a known risk of disease progression, opinion in the medical community is divided regarding screening for carcinoma of the prostate. While both digital rectal examination and PSA screening have demonstrated reasonable performance characteristics (sensitivity, specificity, and positive predictive value) for the early detection of prostate cancer, the lack of evidence that screening and treatment affects ultimate population morbidity or mortality has led many organizations to eschew screening.

The tremendous impact of prostate cancer on the U.S. population, as well as the financial burden of the disease both for patients and society, has led to an increased interest in primary disease prevention.

References

  1. American Cancer Society.: Cancer Facts and Figures 2008. Atlanta, Ga: American Cancer Society, 2008. Also available online. Last accessed October 1, 2008. 

  2. Sakr WA, Haas GP, Cassin BF, et al.: The frequency of carcinoma and intraepithelial neoplasia of the prostate in young male patients. J Urol 150 (2 Pt 1): 379-85, 1993.  [PUBMED Abstract]

  3. Hølund B: Latent prostatic cancer in a consecutive autopsy series. Scand J Urol Nephrol 14 (1): 29-35, 1980.  [PUBMED Abstract]

  4. Ries LAG, Harkins D, Krapcho M, et al.: SEER Cancer Statistics Review, 1975-2003. Bethesda, Md: National Cancer Institute, 2006. Also available online. Last accessed July 31, 2008. 

  5. Horm JW, Sondik EJ: Person-years of life lost due to cancer in the United States, 1970 and 1984. Am J Public Health 79 (11): 1490-3, 1989.  [PUBMED Abstract]

  6. Whitmore WF Jr, Warner JA, Thompson IM Jr: Expectant management of localized prostatic cancer. Cancer 67 (4): 1091-6, 1991.  [PUBMED Abstract]

  7. Orozco R, O'Dowd G, Kunnel B, et al.: Observations on pathology trends in 62,537 prostate biopsies obtained from urology private practices in the United States. Urology 51 (2): 186-95, 1998.  [PUBMED Abstract]

  8. D'Amico AV, Moul J, Carroll PR, et al.: Cancer-specific mortality after surgery or radiation for patients with clinically localized prostate cancer managed during the prostate-specific antigen era. J Clin Oncol 21 (11): 2163-72, 2003.  [PUBMED Abstract]

  9. Gleason DF, Mellinger GT: Prediction of prognosis for prostatic adenocarcinoma by combined histological grading and clinical staging. J Urol 111 (1): 58-64, 1974.  [PUBMED Abstract]

  10. Gleason DF: Histologic grading and clinical staging of prostatic carcinoma. In: Tannenbaum M: Urologic Pathology: The Prostate. Philadelphia, Pa: Lea and Febiger, 1977, pp 171-197. 

  11. Albertsen PC, Hanley JA, Barrows GH, et al.: Prostate cancer and the Will Rogers phenomenon. J Natl Cancer Inst 97 (17): 1248-53, 2005.  [PUBMED Abstract]

  12. Thompson IM, Canby-Hagino E, Lucia MS: Stage migration and grade inflation in prostate cancer: Will Rogers meets Garrison Keillor. J Natl Cancer Inst 97 (17): 1236-7, 2005.  [PUBMED Abstract]

  13. Holmberg L, Bill-Axelson A, Helgesen F, et al.: A randomized trial comparing radical prostatectomy with watchful waiting in early prostate cancer. N Engl J Med 347 (11): 781-9, 2002.  [PUBMED Abstract]

  14. Middleton RG, Thompson IM, Austenfeld MS, et al.: Prostate Cancer Clinical Guidelines Panel Summary report on the management of clinically localized prostate cancer. The American Urological Association. J Urol 154 (6): 2144-8, 1995.  [PUBMED Abstract]

  15. Moul JW: Prostate specific antigen only progression of prostate cancer. J Urol 163 (6): 1632-42, 2000.  [PUBMED Abstract]

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