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Prostate Cancer Treatment (PDQ®)
Patient Version   Health Professional Version   En español   Last Modified: 07/02/2008



Purpose of This PDQ Summary






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Cellular Classification






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Treatment Option Overview






Stage I Prostate Cancer






Stage II Prostate Cancer






Stage III Prostate Cancer






Stage IV Prostate Cancer






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Stage II Prostate Cancer

Current Clinical Trials

Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)

Stage II prostate cancer is defined by the following staging systems:

  • American Joint Committee on Cancer's (AJCC) TNM classification system:
    • T1a, N0, M0, G2–4.
    • T1b, N0, M0, any G.
    • T1c, N0, M0, any G.
    • T1 (not further specified), N0, M0, any G.
    • T2, N0, M0, any G.
  • Jewett staging system: stage A2 or B1 or B2.

 [Note: Previous versions of the AJCC staging system described a tumor’s grade as moderately differentiated, poorly differentiated, or undifferentiated, but these terms are no longer used. G2 is the equivalent of moderately differentiated, and G3–4 is the equivalent of poorly differentiated and undifferentiated.]

Treatment information for patients whose disease has the following TNM classifications:

  • T1a, N0, M0, G2–4.
  • T1b, N0, M0, any G.
  • T1c, N0, M0, any G.
  • T1 (not further specified), N0, M0, any G.
  • T2, N0, M0, G1–2.

A trial has been reported in which 695 men with newly diagnosed well-differentiated or moderately well-differentiated prostate cancers of clinical stages T1b, T1c, or T2 were randomly assigned to receive radical prostatectomy versus watchful waiting.[1] In contrast to prostate cancer patients in the United States, most of the men in this study had been diagnosed clinically, rather than by screening. At a median follow-up of 6.2 years, prostate cancer-specific mortality was 4.6% in the prostatectomy arm of the study versus 8.9% in the watchful waiting arm (P = .02);[1][Level of evidence: 1iiB] however, overall mortality in the two groups was similar (P = .31).[1][Level of evidence: 1iiA] After 10 years, the difference in overall survival (OS) was approximately 73% versus 68%; absolute difference 5.0%; relative risk of death 0.74 (95% confidence interval [CI], 0.56–0.99). This benefit was restricted to men younger than 65 years at the time of surgery (P = .01 in a planned subset analysis of the effect of age on treatment efficacy).[2] A quality-of-life substudy was conducted in 326 of the men in the randomized study.[3] Men filled out questionnaires at a median of about 4 years after study entry. The principal differences in symptoms between the two groups were in sexual and urinary function. In the surgery and watchful waiting groups, 80% versus 45% of the men answering the questionnaire said they seldom or never had erections sufficient for sexual intercourse. Forty-nine percent of men in the prostatectomy arm had urinary leakage at least once a week, 43% used protective aids regularly, and 14% used diapers or urine bags compared to 21%, 10%, and 1%, respectively, in the watchful waiting arm; however, the men on the watchful waiting arm had more obstructive symptoms (e.g., severe symptoms on the American Urologic Symptom Index of 7% in the watchful waiting arm vs. 10% in the prostatectomy arm and moderate symptoms of 42% vs. 24%).[3][Level of evidence: 1iiC]

An older randomized study comparing radical prostatectomy at diagnosis to expectant therapy (careful observation with therapy as needed) in stage I and stage II cancers did not show a statistically significant difference in survival;[4] however, the trial of 95 patients was not large enough to exclude a small but medically significant difference in OS, nor did it include information to measure time to progression, cancer-specific survival, or quality of life.

Often, baseline rates of PSA changes are thought to be markers of tumor progression. Even though a tumor marker or characteristic may be consistently associated with a high risk of prostate cancer progression or death, it may be a very poor predictor and therefore of very limited utility in making therapeutic decisions. For example, baseline PSA and rate of PSA change were associated with subsequent metastasis or prostate cancer death in a cohort of 267 men with clinically localized prostate cancer who were managed by watchful waiting in the control arm of a randomized trial comparing radical prostatectomy to watchful waiting.[5,6] Nevertheless, the accuracy of classifying men into groups whose cancer remained indolent versus those whose cancer progressed was poor at all examined cut points of PSA or PSA rate of change.

Patients with locally advanced nonmetastatic disease (T2–T4, N0–N1, M0) are at risk for developing bone metastases, and bisphosphonates are being studied as a strategy to decrease this risk. However, a placebo-controlled randomized trial (MRC-PRO4) of a 5-year regimen of the first generation bisphosphonate clodronate in high oral doses (2,080 mg per day) had no favorable impact on either time to symptomatic bone metastasis or survival.[7][Level of evidence: 1iA]

Standard treatment options:

  1. Radical prostatectomy, usually with pelvic lymphadenectomy (with or without the nerve-sparing technique designed to preserve potency).[8-10] Radical prostatectomy may be difficult after a transurethral resection of the prostate (TURP). Consideration may be given to postoperative radiation therapy for patients who are found to have capsular penetration or seminal vesicle invasion by tumor at the time of prostatectomy or who have a detectable level of prostate-specific antigen (PSA) more than 3 weeks after surgery.[11-16] Because duration of follow-up in available studies is still relatively short, the value of postoperative radiation therapy is yet to be determined; however, postoperative radiation therapy does reduce local recurrence.[17] Careful treatment planning is necessary to avoid morbidity.[11-16] Clinical trials are in progress.


  2. Careful observation without further immediate treatment in selected patients.[4,18]


  3. External-beam radiation therapy (EBRT).[19-23] Prophylactic radiation therapy to clinically or pathologically uninvolved pelvic lymph nodes does not appear to improve OS or prostate cancer-specific survival as seen in the Radiation Therapy Oncology Group Trial (RTOG-7706) trial, for example.[24][Level of evidence: 1iiA] Although the RTOG-9413 trial showed an increased progression-free survival at 4 years for patients with a 15% estimated risk of lymph node involvement receiving whole-pelvic radiation therapy as compared with prostate-only radiation therapy, OS and PSA failure rates were not significantly different.[25,26][Level of evidence: 1iiDiii] Definitive radiation therapy should be delayed 4 to 6 weeks after TURP to reduce incidence of stricture.[27]


  4. EBRT plus androgen-suppression therapy.[28,29] Three-dimensional–conformal radiation therapy (3D–CRT) (70 Gy) with versus without a total of 6 months of androgen-suppression therapy ([AST]: combined-luteinizing hormone–release hormone [LHRH] plus flutamide) have been compared in a randomized trial of men with clinical stage I or stage II cancer who are at elevated risk for disease progression (i.e., PSA ≥10 mg/ml or Gleason score ≥7).[30] In the trial, 206 patients were randomly assigned and followed for a median of 4.5 years. The estimated 5-year OS rate in the radiation-only arm was 78% (95% CI, 68%–88%) versus 88% (95% CI, 80%–95%) in the radiation-plus AST arm (P = .04).[30][Level of evidence: 1iiA]

    Bicalutamide has not been shown to improve OS in patients with localized or locally advanced prostate cancer. The Early Prostate Cancer (EPC) program is a large, randomized, placebo-controlled, international trial that compared bicalutamide (150 mg orally per day) plus standard care (radical prostatectomy, radiation therapy, or watchful waiting, depending on local custom) with standard care alone for men with nonmetastatic localized or locally advanced prostate cancer (T1–2, N0, NX; T3–4, any N; or any T, N+).[31] Less than 2% of the 8,113 men had known node disease. At a median follow-up of 7.4 years, there was no difference in OS between the bicalutamide and placebo groups (about 76% in both arms [hazard ratio (HR) = 0.99; 95% CI, 0.91–1.09; P = .89]).[31][Level of evidence: 1iA]



  5. Interstitial implantation of radioisotopes (i.e., iodine I 125, palladium, and iridium) done through a transperineal technique with either ultrasound or computed tomography (CT) guidance is being done in carefully selected patients with T1 or T2a tumors. Short-term results in these patients are similar to those for radical prostatectomy or EBRT.[32-34][Level of evidence: 3iiiDiv] One advantage is that the implant is performed as outpatient surgery. The rate of maintenance of sexual potency with interstitial implants has been reported to be 86% to 92%,[32,34] which compares with rates of 10% to 40% with radical prostatectomy and 40% to 60% with EBRT; however, urinary tract frequency, urgency, and less commonly, urinary retention are seen in most patients but subside with time. Rectal ulceration may also be seen. In one series, a 10% 2-year actuarial genitourinary grade 2 complication rate and a 12% risk of rectal ulceration was seen. This risk decreased with increased operator experience and modification of implant technique.[32] Long-term follow-up of these patients is necessary to assess treatment efficacy and side effects.

    Retropubic freehand implantation with iodine I 125 has been associated with an increased local failure and complication rate [35,36] and is now rarely done.



  6. Other clinical trials.


Treatment information for patients whose disease has the following classifications:

  • AJCC's TNM classification system: T2, N0, M0, any G.
  • Jewett staging system: A2 or B1 or B2.

Radical prostatectomy, EBRT, and interstitial implantation of radioisotopes are each employed in the treatment of stage II prostate cancer with apparently similar therapeutic effects. Radical prostatectomy and radiation therapy yield apparently similar survival rates with as many as 10 years of follow-up. For well-selected patients, radical prostatectomy can achieve 15-year survival comparable to an age-matched population without prostate cancer.[18] Unfortunately, randomized comparative trials of these treatment methods with prolonged follow-up are lacking. Patients with a small palpable cancer (T2a, N0, M0) fare better than patients in whom the disease involves both lobes of the gland (T2c, N0, M0). Patients proven free of node metastases by pelvic lymphadenectomy fare better than patients in whom this staging procedure is not performed; however, this is the result of selection of patients who have a more favorable prognosis. Side effects of the various forms of therapy—including impotence, incontinence, and bowel injury—should be considered in determining the type of treatment to employ.

In a retrospective pooled analysis, 828 men with clinically localized prostate cancer were managed by initial conservative therapy with subsequent hormone therapy given at the time of symptomatic disease progression. This study showed that the patients with grade 1 or grade 2 tumors experienced a disease-specific survival of 87% at 10 years and that their OS closely approximated the expected survival among men of similar ages in the general population.[18] The decision to treat should be made in the context of the patient’s age, associated medical illnesses, and personal desires.

The role of adjuvant hormonal therapy in patients with locally advanced disease has been analyzed by the Agency for Health Care Policy and Research (now the Agency for Healthcare Research and Quality). Most patients have more advanced disease, but patients with bulky T2b to T2c tumors were included in the study groups that were re-evaluating the role of adjuvant hormonal therapy in patients with locally advanced disease. Randomized clinical trial evidence comparing radiation therapy to radiation therapy with prolonged androgen suppression has been published. The meta-analysis found a difference in 5-year OS in favor of radiation therapy plus continued androgen suppression (LHRH agonist or orchiectomy) compared to radiation therapy alone (HR = 0.631; 95% CI, 0.479–0.831).[37][Level of evidence: 1iiA]

Likewise, a meta-analysis of seven randomized controlled trials comparing early (adjuvant or neoadjuvant) to deferred hormonal treatment (LHRH agonists and/or antiandrogens) in patients with locally advanced prostate cancer, whether treated by prostatectomy, radiation therapy, or watchful waiting, showed improved overall mortality (RR=0.86; 95% CI, 0.82–0.91).[38][Level of evidence: 1iiA]

Bicalutamide has not been shown to improve OS in patients with localized or locally advanced prostate cancer. The EPC program is a large, randomized, placebo-controlled, international trial that compared bicalutamide (150 mg orally per day) plus standard care (radical prostatectomy, radiation therapy, or watchful waiting, depending on local custom) with standard care alone for men with nonmetastatic localized or locally advanced prostate cancer (T1–2, N0, NX; T3–4, any N; or any T, N+).[31] Less than 2% of the 8,113 men had known node disease. At a median follow-up of 7.4 years, there was no difference in OS between the bicalutamide and placebo groups (about 76% in both arms [HR = 0.99; 95% CI, 0.91–1.09; P = .89]).[31][Level of evidence: 1iA]

Patients with locally advanced nonmetastatic disease (T2–T4, N0–N1, M0) are at risk for developing bone metastases, and bisphosphonates are being studied as a strategy to decrease this risk. However, a placebo-controlled randomized trial (MRC-PRO4) of a 5-year regimen of the first generation bisphosphonate clodronate in high oral doses (2,080 mg per day) had no favorable impact on either time to symptomatic bone metastasis or survival.[7][Level of evidence: 1iA]

Standard treatment options:

  1. Radical prostatectomy usually with pelvic lymphadenectomy.[8,9,39,40] If allowed by the extent of tumor, anatomical dissection that preserves nerves necessary for erection may avoid impotence postoperatively in some patients.[10,39] Since about 40% to 50% of men with clinically organ-confined disease are found to have pathologic extension beyond the prostate capsule or surgical margins (i.e., pathologic stage III disease), the role of postprostatectomy adjuvant radiation therapy has been studied. In a randomized trial of 425 men with pathologic T3, N0, M0 disease, postsurgical EBRT (60 Gy–64 Gy to the pelvic fossa over 30–32 fractions) was compared to observation.[41] The primary endpoint was metastasis-free survival, an endpoint that could be affected by serial PSA monitoring and resulting metastatic work-up for PSA increase. This could have biased the primary endpoint in favor of radiation therapy, which was associated with a lower rate of PSA rise. Nevertheless, metastasis-free survival was not statistically different between the two study arms (P = .06). After a median follow-up of 10.6 years, the median survival was 14.7 years in the radiation therapy group versus 13.8 years in the observation group (P = .16).[41][Level of evidence: 1iiA] Although the survival rates were not statistically different, complication rates were substantially higher in the radiation therapy group: overall complications were 23.8% versus 11.9%, rectal complications were 3.3% versus 0%, and urethral stricture was 17.8% versus 9.5%, respectively. Postoperative radiation therapy does reduce local recurrence.[17] The role of preoperative (neoadjuvant) hormonal therapy is not established.[42,43] Also, the morphologic changes induced by neoadjuvant androgen ablation may complicate assessment of surgical margins and capsular involvement.[44]


  2. EBRT.[19-23,45] Prophylactic radiation therapy to clinically or pathologically uninvolved pelvic lymph nodes does not appear to improve OS or prostate cancer-specific survival.[24][Level of evidence: 1iiA] Definitive radiation therapy should be delayed 4 to 6 weeks after TURP to reduce incidence of stricture.[27] For patients with bulky T2b to T2c tumors, adjuvant hormonal therapy should be considered.[37]


  3. EBRT plus androgen suppression therapy.[28,29]


  4. Careful observation without further immediate treatment (in selected patients).[4,18]


  5. Interstitial implantation of radioisotopes (i.e., iodine I 125, palladium, and iridium) done through a transperineal technique with either ultrasound or CT guidance is being done in carefully selected patients with T1 or T2a tumors. Short-term results in these carefully selected patients are similar to those for radical prostatectomy or EBRT.[32-34][Level of evidence: 3iiiDiv] One advantage is that the implant is performed as outpatient surgery. The rate of maintenance of sexual potency with interstitial implants has been reported to be 86% to 92%,[32,46] which compares with rates of 10% to 40% with radical prostatectomy and 40% to 60% with EBRT; however, urinary tract frequency, urgency, or less commonly, urinary retention are seen in most patients but subside with time. Rectal ulceration may also be seen. In one series, a 10% 2-year actuarial genitourinary grade 2 complication rate, and a 12% risk of rectal ulceration was seen. This risk decreased with increased operator experience and modification of implant technique.[32] Long-term follow-up of these patients is necessary to assess treatment efficacy and side effects.

    Retropubic freehand implantation with iodine I 125 has been associated with an increased local failure and complication rate [35,36] and is now rarely done.



  6. EBRT designed to decrease exposure of normal tissues using methods such as CT-based 3-D conformal treatment planning is under clinical evaluation.[47]


  7. Ultrasound-guided percutaneous cryosurgery is under clinical evaluation.

    Cryosurgery is a surgical technique under development that involves destruction of prostate cancer cells by intermittent freezing of the prostate tissue with cryoprobes and is followed by thawing.[48][Level of evidence: 3iiiC][49,50][Level of evidence: 3iiiDiv] Cryosurgery is less well established than standard prostatectomy, and long-term outcomes are not as well established as with prostatectomy or radiation therapy. Serious toxic effects include bladder outlet injury, urinary incontinence, sexual impotence, and rectal injury. The technique of cryosurgery is under development. Impotence is common. The frequency of other side effects and the probability of cancer control at 5 years' follow-up have varied among reporting centers, and series are small compared with surgery and radiation therapy.[49,50]



  8. Other clinical trials, including trials of neoadjuvant hormonal therapy followed by radical prostatectomy.[51,52]


Current Clinical Trials

Check for U.S. clinical trials from NCI's PDQ Cancer Clinical Trials Registry that are now accepting patients with stage II prostate cancer. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References

  1. 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]

  2. Bill-Axelson A, Holmberg L, Ruutu M, et al.: Radical prostatectomy versus watchful waiting in early prostate cancer. N Engl J Med 352 (19): 1977-84, 2005.  [PUBMED Abstract]

  3. Steineck G, Helgesen F, Adolfsson J, et al.: Quality of life after radical prostatectomy or watchful waiting. N Engl J Med 347 (11): 790-6, 2002.  [PUBMED Abstract]

  4. Graversen PH, Nielsen KT, Gasser TC, et al.: Radical prostatectomy versus expectant primary treatment in stages I and II prostatic cancer. A fifteen-year follow-up. Urology 36 (6): 493-8, 1990.  [PUBMED Abstract]

  5. Fall K, Garmo H, Andrén O, et al.: Prostate-specific antigen levels as a predictor of lethal prostate cancer. J Natl Cancer Inst 99 (7): 526-32, 2007.  [PUBMED Abstract]

  6. Parekh DJ, Ankerst DP, Thompson IM: Prostate-specific antigen levels, prostate-specific antigen kinetics, and prostate cancer prognosis: a tocsin calling for prospective studies. J Natl Cancer Inst 99 (7): 496-7, 2007.  [PUBMED Abstract]

  7. Mason MD, Sydes MR, Glaholm J, et al.: Oral sodium clodronate for nonmetastatic prostate cancer--results of a randomized double-blind placebo-controlled trial: Medical Research Council PR04 (ISRCTN61384873). J Natl Cancer Inst 99 (10): 765-76, 2007.  [PUBMED Abstract]

  8. Zincke H, Bergstralh EJ, Blute ML, et al.: Radical prostatectomy for clinically localized prostate cancer: long-term results of 1,143 patients from a single institution. J Clin Oncol 12 (11): 2254-63, 1994.  [PUBMED Abstract]

  9. Catalona WJ, Bigg SW: Nerve-sparing radical prostatectomy: evaluation of results after 250 patients. J Urol 143 (3): 538-43; discussion 544, 1990.  [PUBMED Abstract]

  10. Catalona WJ, Basler JW: Return of erections and urinary continence following nerve sparing radical retropubic prostatectomy. J Urol 150 (3): 905-7, 1993.  [PUBMED Abstract]

  11. Lange PH, Reddy PK, Medini E, et al.: Radiation therapy as adjuvant treatment after radical prostatectomy. NCI Monogr (7): 141-9, 1988.  [PUBMED Abstract]

  12. Ray GR, Bagshaw MA, Freiha F: External beam radiation salvage for residual or recurrent local tumor following radical prostatectomy. J Urol 132 (5): 926-30, 1984.  [PUBMED Abstract]

  13. Carter GE, Lieskovsky G, Skinner DG, et al.: Results of local and/or systemic adjuvant therapy in the management of pathological stage C or D1 prostate cancer following radical prostatectomy. J Urol 142 (5): 1266-70; discussion 1270-1, 1989.  [PUBMED Abstract]

  14. Freeman JA, Lieskovsky G, Cook DW, et al.: Radical retropubic prostatectomy and postoperative adjuvant radiation for pathological stage C (PcN0) prostate cancer from 1976 to 1989: intermediate findings. J Urol 149 (5): 1029-34, 1993.  [PUBMED Abstract]

  15. Stamey TA, Yang N, Hay AR, et al.: Prostate-specific antigen as a serum marker for adenocarcinoma of the prostate. N Engl J Med 317 (15): 909-16, 1987.  [PUBMED Abstract]

  16. Hudson MA, Bahnson RR, Catalona WJ: Clinical use of prostate specific antigen in patients with prostate cancer. J Urol 142 (4): 1011-7, 1989.  [PUBMED Abstract]

  17. Paulson DF, Moul JW, Walther PJ: Radical prostatectomy for clinical stage T1-2N0M0 prostatic adenocarcinoma: long-term results. J Urol 144 (5): 1180-4, 1990.  [PUBMED Abstract]

  18. Chodak GW, Thisted RA, Gerber GS, et al.: Results of conservative management of clinically localized prostate cancer. N Engl J Med 330 (4): 242-8, 1994.  [PUBMED Abstract]

  19. Bagshaw MA: External radiation therapy of carcinoma of the prostate. Cancer 45 (7 Suppl): 1912-21, 1980.  [PUBMED Abstract]

  20. Forman JD, Zinreich E, Lee DJ, et al.: Improving the therapeutic ratio of external beam irradiation for carcinoma of the prostate. Int J Radiat Oncol Biol Phys 11 (12): 2073-80, 1985.  [PUBMED Abstract]

  21. Ploysongsang S, Aron BS, Shehata WM, et al.: Comparison of whole pelvis versus small-field radiation therapy for carcinoma of prostate. Urology 27 (1): 10-6, 1986.  [PUBMED Abstract]

  22. Pilepich MV, Bagshaw MA, Asbell SO, et al.: Definitive radiotherapy in resectable (stage A2 and B) carcinoma of the prostate--results of a nationwide overview. Int J Radiat Oncol Biol Phys 13 (5): 659-63, 1987.  [PUBMED Abstract]

  23. Amdur RJ, Parsons JT, Fitzgerald LT, et al.: The effect of overall treatment time on local control in patients with adenocarcinoma of the prostate treated with radiation therapy. Int J Radiat Oncol Biol Phys 19 (6): 1377-82, 1990.  [PUBMED Abstract]

  24. Asbell SO, Martz KL, Shin KH, et al.: Impact of surgical staging in evaluating the radiotherapeutic outcome in RTOG #77-06, a phase III study for T1BN0M0 (A2) and T2N0M0 (B) prostate carcinoma. Int J Radiat Oncol Biol Phys 40 (4): 769-82, 1998.  [PUBMED Abstract]

  25. Roach M 3rd, DeSilvio M, Lawton C, et al.: Phase III trial comparing whole-pelvic versus prostate-only radiotherapy and neoadjuvant versus adjuvant combined androgen suppression: Radiation Therapy Oncology Group 9413. J Clin Oncol 21 (10): 1904-11, 2003.  [PUBMED Abstract]

  26. Pollack A: A call for more with a desire for less: pelvic radiotherapy with androgen deprivation in the treatment of prostate cancer. J Clin Oncol 21 (10): 1899-901, 2003.  [PUBMED Abstract]

  27. Seymore CH, el-Mahdi AM, Schellhammer PF: The effect of prior transurethral resection of the prostate on post radiation urethral strictures and bladder neck contractures. Int J Radiat Oncol Biol Phys 12 (9): 1597-600, 1986.  [PUBMED Abstract]

  28. Kumar S, Shelley M, Harrison C, et al.: Neo-adjuvant and adjuvant hormone therapy for localised and locally advanced prostate cancer. Cochrane Database Syst Rev (4): CD006019, 2006.  [PUBMED Abstract]

  29. D'Amico AV, Chen MH, Renshaw AA, et al.: Androgen suppression and radiation vs radiation alone for prostate cancer: a randomized trial. JAMA 299 (3): 289-95, 2008.  [PUBMED Abstract]

  30. D'Amico AV, Manola J, Loffredo M, et al.: 6-month androgen suppression plus radiation therapy vs radiation therapy alone for patients with clinically localized prostate cancer: a randomized controlled trial. JAMA 292 (7): 821-7, 2004.  [PUBMED Abstract]

  31. McLeod DG, Iversen P, See WA, et al.: Bicalutamide 150 mg plus standard care vs standard care alone for early prostate cancer. BJU Int 97 (2): 247-54, 2006.  [PUBMED Abstract]

  32. Wallner K, Roy J, Harrison L: Tumor control and morbidity following transperineal iodine 125 implantation for stage T1/T2 prostatic carcinoma. J Clin Oncol 14 (2): 449-53, 1996.  [PUBMED Abstract]

  33. D'Amico AV, Coleman CN: Role of interstitial radiotherapy in the management of clinically organ-confined prostate cancer: the jury is still out. J Clin Oncol 14 (1): 304-15, 1996.  [PUBMED Abstract]

  34. Ragde H, Blasko JC, Grimm PD, et al.: Interstitial iodine-125 radiation without adjuvant therapy in the treatment of clinically localized prostate carcinoma. Cancer 80 (3): 442-53, 1997.  [PUBMED Abstract]

  35. Kuban DA, el-Mahdi AM, Schellhammer PF: I-125 interstitial implantation for prostate cancer. What have we learned 10 years later? Cancer 63 (12): 2415-20, 1989.  [PUBMED Abstract]

  36. Fuks Z, Leibel SA, Wallner KE, et al.: The effect of local control on metastatic dissemination in carcinoma of the prostate: long-term results in patients treated with 125I implantation. Int J Radiat Oncol Biol Phys 21 (3): 537-47, 1991.  [PUBMED Abstract]

  37. Seidenfeld J, Samson DJ, Aronson N, et al.: Relative effectiveness and cost-effectiveness of methods of androgen suppression in the treatment of advanced prostate cancer. Evid Rep Technol Assess (Summ) (4): i-x, 1-246, I1-36, passim, 1999.  [PUBMED Abstract]

  38. Boustead G, Edwards SJ: Systematic review of early vs deferred hormonal treatment of locally advanced prostate cancer: a meta-analysis of randomized controlled trials. BJU Int 99 (6): 1383-9, 2007.  [PUBMED Abstract]

  39. Eastham JA, Scardino PT: Radical prostatectomy. In: Walsh PC, Retik AB, Vaughan ED, et al., eds.: Campbell's Urology. 8th ed. Philadelphia: Saunders, 2002, pp 3080-3083. 

  40. Paulson DF, Lin GH, Hinshaw W, et al.: Radical surgery versus radiotherapy for adenocarcinoma of the prostate. J Urol 128 (3): 502-4, 1982.  [PUBMED Abstract]

  41. Thompson IM Jr, Tangen CM, Paradelo J, et al.: Adjuvant radiotherapy for pathologically advanced prostate cancer: a randomized clinical trial. JAMA 296 (19): 2329-35, 2006.  [PUBMED Abstract]

  42. Witjes WP, Schulman CC, Debruyne FM: Preliminary results of a prospective randomized study comparing radical prostatectomy versus radical prostatectomy associated with neoadjuvant hormonal combination therapy in T2-3 N0 M0 prostatic carcinoma. The European Study Group on Neoadjuvant Treatment of Prostate Cancer. Urology 49 (3A Suppl): 65-9, 1997.  [PUBMED Abstract]

  43. Fair WR, Cookson MS, Stroumbakis N, et al.: The indications, rationale, and results of neoadjuvant androgen deprivation in the treatment of prostatic cancer: Memorial Sloan-Kettering Cancer Center results. Urology 49 (3A Suppl): 46-55, 1997.  [PUBMED Abstract]

  44. Bazinet M, Zheng W, Bégin LR, et al.: Morphologic changes induced by neoadjuvant androgen ablation may result in underdetection of positive surgical margins and capsular involvement by prostatic adenocarcinoma. Urology 49 (5): 721-5, 1997.  [PUBMED Abstract]

  45. Perez CA, Garcia D, Simpson JR, et al.: Factors influencing outcome of definitive radiotherapy for localized carcinoma of the prostate. Radiother Oncol 16 (1): 1-21, 1989.  [PUBMED Abstract]

  46. Blasko JC, Wallner K, Grimm PD, et al.: Prostate specific antigen based disease control following ultrasound guided 125iodine implantation for stage T1/T2 prostatic carcinoma. J Urol 154 (3): 1096-9, 1995.  [PUBMED Abstract]

  47. Hanks GE, Hanlon AL, Schultheiss TE, et al.: Dose escalation with 3D conformal treatment: five year outcomes, treatment optimization, and future directions. Int J Radiat Oncol Biol Phys 41 (3): 501-10, 1998.  [PUBMED Abstract]

  48. Robinson JW, Saliken JC, Donnelly BJ, et al.: Quality-of-life outcomes for men treated with cryosurgery for localized prostate carcinoma. Cancer 86 (9): 1793-801, 1999.  [PUBMED Abstract]

  49. Donnelly BJ, Saliken JC, Ernst DS, et al.: Prospective trial of cryosurgical ablation of the prostate: five-year results. Urology 60 (4): 645-9, 2002.  [PUBMED Abstract]

  50. Aus G, Pileblad E, Hugosson J: Cryosurgical ablation of the prostate: 5-year follow-up of a prospective study. Eur Urol 42 (2): 133-8, 2002.  [PUBMED Abstract]

  51. Fair WR, Cookson MS, Stroumbakis N, et al.: Update on neoadjuvant androgen deprivation therapy (ADT) and radical prostatectomy in localized prostate cancer. [Abstract] Proceedings of the American Urological Association 155(Suppl): A-1426, 667A, 1996. 

  52. Soloway MS, Sharifi R, Wajsman Z, et al.: Randomized prospective study: radical prostatectomy alone vs radical prostatectomy preceded by androgen blockade in cT2b prostate cancer - initial results. [Abstract] Proceedings of the American Urological Association 155(Suppl): A-976, 555A, 1996. 

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