Medscape is available in 5 Language Editions – Choose your Edition here.


Prostate Cancer

  • Author: Gerald W Chodak, MD; Chief Editor: Edward David Kim, MD, FACS  more...
Updated: Oct 15, 2015

Practice Essentials

Prostate cancer is the most common noncutaneous cancer in men in the United States. An estimated one in six white men and one in five African-American men will be diagnosed with prostate cancer in their lifetime, with the likelihood increasing with age.

The image below depicts the anatomy of the male pelvis and genitourinary tract.

Management of localized prostate cancer. This diag Management of localized prostate cancer. This diagram depicts the relevant anatomy of the male pelvis and genitourinary tract.

See Prostate Cancer: Diagnosis and Staging, a Critical Images slideshow, to help determine the best diagnostic approach for this potentially deadly disease.

See Advanced Prostate Cancer: Signs of Metastatic Disease, a Critical Images slideshow, for help identifying the signs of metastatic disease.

Signs and symptoms

Currently, most cases of prostate cancer are identified by screening in asymptomatic men. Symptoms of prostate cancer include the following:

  • Urinary complaints or retention
  • Back pain
  • Hematuria

However, such symptoms are often from diseases other than prostate cancer (eg, urinary complaints from benign prostatic hyperplasia [BPH]). Physical examination alone cannot reliably differentiate benign prostatic disease from cancer.

Findings in patients with advanced disease may include the following:

  • Cancer cachexia
  • Bony tenderness
  • Lower-extremity lymphedema or deep venous thrombosis
  • Adenopathy
  • Overdistended bladder due to outlet obstruction

See Clinical Presentation for more detail.


Elevated prostate-specific antigen (PSA) level

  • No PSA level guarantees the absence of prostate cancer.
  • The risk of disease increases as the PSA level increases, from about 8% with a PSA level of 1 ng/mL to about 25% with a PSA level of 4-10 ng/mL. [1]

Abnormal digital rectal examination (DRE) findings

  • DRE is examiner-dependent, and serial examinations over time are best
  • Most patients diagnosed with prostate cancer have normal DRE results but abnormal PSA readings


  • Biopsy establishes the diagnosis
  • False-negative results often occur, so multiple biopsies may be needed before prostate cancer is detected


The American Cancer Society (ACS) recommends that men decide whether to be screened for prostate cancer based on a discussion with their health care provider about the uncertainties, risks, and potential benefits of screening.[2]

The recommended age for starting screening is as follows:

  • 50 years of age for men at average risk who have at least a 10-year life expectancy
  • 40 or 45 years of age for African Americans and men who have had a first-degree relative diagnosed with prostate cancer before age 65 years
  • 40 years of age for men with several first-degree relatives who had prostate cancer at an early age

The US Preventive Services Task Force (USPSTF) recommends against any routine PSA-based screening for prostate cancer.[3] This recommendation is considered controversial.[4]

See Workup for more detail.


Localized prostate cancer

Standard treatments for clinically localized prostate cancer include the following:

  • Radical prostatectomy
  • Radiation therapy
  • Active surveillance
  • Androgen deprivation therapy (ADT)

Metastatic prostate cancer

Metastatic prostate cancer is rarely curable, and management of these cases typically involves the following:

  • Therapy directed at relief of particular symptoms (eg, palliation of pain)
  • Attempts to slow further progression of disease

See Treatment and Medication for more detail.



Prostate cancer is the most common noncutaneous cancer in men. Although prostate cancer can be a slow-growing cancer, thousands of men die of the disease each year. It is the second most common cause of cancer death in males (see Epidemiology).

Marked variation in rates of prostate cancer among populations in different parts of the world suggests the involvement of genetic factors. Familial predisposition also occurs. Environmental factors, notably diet, are also important (see Etiology).

Currently, the majority of prostate cancers are identified in patients who are asymptomatic. Diagnosis in such cases is based on abnormalities in a screening prostate-specific antigen (PSA) level or findings on digital rectal examination (see Presentation and Workup).

Screening for prostate cancer is a controversial topic, in large part because of the conflicting findings from prospective, randomized studies (see Workup). Education about the risks and benefits is important to help men make informed decisions regarding screening and, in those diagnosed with prostate cancer, the various treatment options (see Treatment). (See the image below.)

The standard approach for grading prostate cancer The standard approach for grading prostate cancer depends on a Gleason score, which is based on pathologic evaluation of a prostatectomy specimen and is commonly estimated from prostate biopsy tissue. Prostate cancer patterns are assigned a number from 1-5; the score is created by adding the most common pattern and the highest-grade patterns.

See also the following Medscape articles:



The prostate lies below the bladder and encompasses the prostatic urethra. It is surrounded by a capsule and is separated from the rectum by a layer of fascia termed the Denonvilliers aponeurosis. (See the image below.)

Management of localized prostate cancer. This diag Management of localized prostate cancer. This diagram depicts the relevant anatomy of the male pelvis and genitourinary tract.

The inferior vesical artery, which is derived from the internal iliac artery, supplies blood to the base of the bladder and prostate. The capsular branches of the inferior vesical artery help to identify the pelvic plexus arising from the S2-4 and T10-12 nerve roots. The neurovascular bundle lies on either side of the prostate on the rectum. It is derived from the pelvic plexus and is important for erectile function.



Prostate cancer develops when the rates of cell division and cell death are no longer equal, leading to uncontrolled tumor growth. Following the initial transformation event, further mutations of a multitude of genes, including the genes for p53 and retinoblastoma, can lead to tumor progression and metastasis. Most prostate cancers (95%) are adenocarcinomas.

Approximately 4% of cases of prostate cancer have transitional cell morphology and are thought to arise from the urothelial lining of the prostatic urethra. The few cases that have neuroendocrine morphology are believed to arise from the neuroendocrine stem cells normally present in the prostate or from aberrant differentiation programs during cell transformation.

Squamous cell carcinomas constitute less than 1% of all prostate carcinomas. In many cases, prostate carcinomas with squamous differentiation arise after radiation or hormone treatment.

Of prostate cancer cases, 70% arise in the peripheral zone, 15-20% arise in the central zone, and 10-15% arise in the transitional zone. Most prostate cancers are multifocal, with synchronous involvement of multiple zones of the prostate, which may be due to clonal and nonclonal tumors.

Local spread and metastasis

When these cancers are locally invasive, the transitional-zone tumors spread to the bladder neck, while the peripheral-zone tumors extend into the ejaculatory ducts and seminal vesicles. Penetration through the prostatic capsule and along the perineural or vascular spaces occurs relatively late.

The mechanism for distant metastasis is poorly understood. The cancer spreads to bone early, often without significant lymphadenopathy. Currently, 2 predominant theories have been proposed for spread: the mechanical theory and the seed-and-soil theory.

The mechanical theory attributes metastasis to direct spread through the lymphatics and venous spaces into the lower lumbar spine. Advocates of the seed-and-soil theory, however, believe that tissue factors that allow for preferential growth in certain tissues, such as bone, must be present. Lung, liver, and adrenal metastases have also been documented. Specific tissue growth factors and extracellular matrices are possible examples.

The doubling time in early stage disease is variable. In the majority of cases, doubling time is longer than 4 years. Only a small percentage of prostate cancers double in less than 2 years. Doubling time tends to accelerate as the tumor grows and becomes more aggressive. Larger tumors usually have a higher Gleason grade and a faster doubling time.

The natural history of clinically localized disease varies, with lower-grade tumors having a more indolent course and some high-grade lesions progressing to metastatic disease with relative rapidity. Given the typically slow progression of localized disease, several studies have examined the strategy of active surveillance in selected groups of patients.[5]



Marked variation in rates of prostate cancer among populations in different parts of the world suggests the involvement of genetic factors. For example, the risk of prostate cancer is particularly high in people of sub-Saharan African ancestry, while the risk tends to be low in many Asian populations. Increased risk in Asians who have migrated to the United States suggests the importance of environmental factors, notably diet.[1] Familial predisposition also occurs.

Prostate cancer is also found during autopsies performed in men with other causes of death. The rate of this latent or autopsy cancer is much greater than that of clinical cancer. In fact, it may be as high as 80% by age 80 years. Interestingly, the prevalence of the latent or autopsy form of the disease is similar worldwide. Together with migration studies, this suggests that environmental factors play a significant promoting role in the development of a clinical cancer from a latent precursor.


Studies in different populations have identified several variants in the 8q24 region on chromosome 8 that are associated with increased risk of prostate cancer.[6] Gene alterations on chromosome 1, chromosome 17, and the X chromosome have been found in some patients with a family history of prostate cancer. The HPC1 (hereditary prostate cancer 1) gene and the PCAP (predisposing for cancer of the prostate) gene are on chromosome 1, while the human prostate cancer gene is on the X chromosome.

Genetic studies suggest that a strong familial predisposition may be responsible for as many as 5-10% of prostate cancer cases. Men with a family history of prostate cancer have a higher risk of developing prostate cancer and are also likely to present 6-7 years earlier. Several reports have suggested a shared familial risk (inherited or environmental) for prostate and breast cancer. BRCA-2 mutations increase the risk for prostate cancer that is more aggressive and develops at a younger age.[1]

A study by Ewing et al found that germline mutations in HOXB13 may be a risk factor for prostate cancer. HOXB13 is a homeobox transcription factor gene that is important in prostate development. The G84E variant of this gene, while rare, is significantly more common in men with early onset, familial prostate cancer than in those with late-onset, nonfamilial prostate cancer.[7]

An examination of cancer histories of 198 Lynch syndrome families, including probands and their first- through fourth-degree relatives, found that men with Lynch syndrome have a two-fold increased risk of prostate cancer compared to the general population. Of the 4127 men involved in the study, 97 had prostate cancer. Median age at diagnosis was 65, with 11.5% diagnosed before age 50. The cumulative risk of prostate cancer for men with Lynch syndrome was 6.3% at age 60 and 30% at age 80, vs a population risk of 2.6% and 17.8%, respectively.[8, 9]


Diet may play a role in the development of prostate cancer. Epidemiologic studies have suggested a variety of dietary factors that may be associated with the disease, particularly fat intake and obesity. See Prostate Cancer and Nutrition for a complete discussion of this topic.


Hormonal causes of prostate cancer have also been postulated. Androgen ablation causes a regression of prostate cancer. In addition, as indirect evidence of hormonal causes, eunuchs do not develop adenocarcinoma of the prostate.

Hsing and Comstock performed a large study comparing patients with prostate cancer with controls and found no significant difference in levels of testosterone, dihydrotestosterone, prolactin, follicle-stimulating hormone, or estrone. However, elevated levels of luteinizing hormone and of testosterone:dihydrotestosterone ratios were associated with mildly increased risk.[10]

5-alpha reductase

The Prostate Cancer Prevention Trial studied the prevalence of prostate cancer in a control group and in a group given a 5-alpha-reductase inhibitor (finasteride).[11] While the 5-alpha reductase inhibitor appeared to decrease the prevalence of tumors, some of those that did arise appeared histologically more aggressive. Only long-term follow-up of these patients will determine whether this more aggressive histology accurately reflects the underlying biology of these tumors or whether it is an artifact of the treatment.

A similar study was performed with dutasteride, a molecule that blocks not only D1 but also D2 receptors in the prostate. The investigators found a 22.8% relative risk reduction in the development of prostate cancer, but the study did not fully refute the concern that more aggressive cancers could arise in treated patients.

Possibly for this reason, when the concept of 5-alpha reductase for chemoprevention of prostate cancer was brought before the US Food and Drug Administration (FDA) in 2010, the FDA did not approve the drugs for this indication.[12, 13] Indeed, on June 9, 2011 the FDA announced revisions to the prescribing information for 5-alpha reductase inhibitors to include a warning regarding an increased incidence of high-grade prostate cancer in men taking dutasteride or finasteride compared with placebo.[14]



Internationally, the incidence of prostate cancer varies by more than 50-fold, with the highest rates being in North America, Australia, and northern and central Europe and the lowest rates being in southeastern and south-central Asia and northern Africa.[1]

Occurrence in the United States

In the United States, prostate cancer is the most common noncutaneous cancer in men. An estimated one in six white men and one in five African American men will be diagnosed with prostate cancer in their lifetime, with the likelihood increasing with age. The American Cancer Society estimates that 220,800 new cases of prostate cancer will be diagnosed in 2015.[15] Prostate cancer is rarely diagnosed in men younger than 40 years, and it is uncommon in men younger than 50 years.

Between 1989 and 1992, incidence rates of prostate cancer increased dramatically in the United States, probably because of earlier diagnoses in asymptomatic men were being made as a result of the increased use of serum PSA testing. In addition, the incidence of organ-confined disease at diagnosis has increased because PSA testing and standard digital rectal examination are performed. Since 1992, incidence rates have declined markedly, decreasing from almost 250 per 100,000 population in 1992 to less than 150 per 100,000 population in 2011.[15]

Racial demographics

Prevalence rates of prostate cancer remain significantly higher in African-American men than in white men, while the prevalence in Hispanic men is similar to that of white men. The prevalence in men of Asian origin is lower than in whites. Although mortality rates are continuing to decline among white and African-American men, mortality rates in African-American men remain more than twice as high as in any other racial group.[15]

Hispanic men and African-American men present with more advanced disease.[16] Studies have found that young African-American men have testosterone levels that are 15% higher than in young white men. Furthermore, evidence indicates that 5-alpha reductase may be more active in African Americans than in whites, implying that hormonal differences may play a role. However, the independent contribution of race is difficult to isolate from the effects of health-care access, income, education, and insurance status.



The most important and established indicators of prognosis for prostate carcinoma include the Gleason grade, the extent of tumor volume, and the presence of capsular penetration or margin positivity at the time of prostatectomy. High-grade prostate cancer, particularly the percentage of Gleason grades 4 and 5 that are present, is associated with adverse pathologic findings and disease progression. Conversely, low-grade prostate tumors are infrequently dangerous.

In a review of 11,521 patients treated with radical prostatectomy at 4 academic centers from 1987 to 2005, Eggener et al reported an overall 15-year prostate cancer–specific mortality rate of 7%. High-grade cancer and seminal vesicle invasion were the prime determinants of prostate cancer–specific mortality.[17]

Despite the steady decline in the incidence of newly diagnosed metastatic prostate cancer and microscopic lymph node metastasis, from 20% in the 1970s to 3.4% in the 1990s, the risk of extra-prostatic disease in patients with clinically localized disease remains high at approximately 30%. Depending on the PSA value, pathologic stage, and histologic grade of the tumor, approximately 30% of patients with clinically localized prostate cancer are estimated to progress despite initial treatment with intent to cure.

The Cancer of the Prostate Risk Assessment (CAPRA) score for predicting prognosis is calculated on the basis of the following:

  • PSA level
  • Gleason score
  • Percentage of biopsy cores positive for cancer
  • Clinical tumor stage
  • Age at diagnosis

In a study of 10,627 men with clinically localized prostate cancer who underwent primary radical prostatectomy, radiation therapy, androgen deprivation monotherapy, or watchful waiting/active surveillance, and had at least 6 months of follow-up after treatment, Cooperberg et al found that the CAPRA score was accurate for predicting metastases, cancer-specific mortality, and all-cause mortality.[18]

In a retrospective study of patients who underwent radical retropubic prostatectomies, researchers found an association between an opioid-sparing approach to anesthesia and reductions in prostate cancer progression and overall mortality. The investigators reviewed 1642 procedures performed with general anesthesia and 1642 prostatectomies performed with an opioid-sparing approach (general anesthesia supplemented with a neuraxial block), in patients diagnosed with prostate cancer between 1991 and 2005. Median follow-up in the study was 9 years.[19, 20] Results indicated that the risk of systemic progression of prostate cancer was almost 3 times greater and the mortality risk was 30% higher in the general anesthesia patients than in patients anesthetized with an opioid-sparing approach.[19, 20]

In a multivariate analysis, biochemical recurrence and disease-specific mortality were much higher in men who were smokers at the time of diagnosis versus those who had never smoked. A higher number of pack-years was associated with significantly increased risk for prostate cancer mortality but not for biochemical recurrence. Men who had quit smoking 10 years prior to diagnosis—or who had quit more recently but smoked for < 20 pack-years—had prostate cancer–mortality risks much like those of men who had never smoked.[21]

In a retrospective study at Johns Hopkins Medical Center in Baltimore, a greater connection between cigarette smoking and risk of prostate cancer recurrence was identified in men who had been treated with radical prostatectomy.[22] Without prospective studies, however, these relationships remain hypothetical.

In an analysis of two large cohort studies of health professionals, researchers found a significantly increased risk for melanoma among men with prostate cancer. In 42,372 participants in the Health Professionals’ Follow-Up Study, a history of prostate cancer was independently associated with an increased risk for melanoma (hazard ratio, 1.83). This association was confirmed in an analysis of 18,603 participants in the Physicians’ Health Study (hazard ratio, 2.17).[23, 24]

Molecular prognostic markers

Several molecular markers have been shown to aid in determining the prognosis of patients undergoing treatment for localized and metastatic prostate cancers. Genetic changes associated with poor survival in prostate cancer include the following[25] :

  • Loss of one or both copies of the tumor suppressor gene PTEN
  • TMPRSS2–ERG chromosome fusion (fusion of an androgen-responsive promoter with the ERG transcription factor)
  • P53 mutations
  • Overexpression of MYC

Assessments of molecular alterations of gene products of RB, BCL2, cathepsin-D, and CDH1, among many others, have also been reported. Decreased expression of the cell cycle inhibitor p27 in prostate cancer cells has been associated with increased risk of prostate cancer recurrence.[18]

Prospective trials are needed to assess these markers more thoroughly before their implementation in clinical management is recommended. Currently, none of them are measured in routine practice.

Prognostic nomograms

The Partin tables are the best nomogram for predicting prostate cancer spread prior to therapy. The tables were updated by experts at Johns Hopkins in January 2013. Updates to the tool were based on a study of 5629 men who underwent radical prostatectomy and staging lymphadenectomy between 2006 and 2011. The updated tables show that certain categories of men who were previously not thought to have a good prognosis (eg, those with a Gleason score of 8) actually can be cured with surgery.[26, 27]

In addition, a series of nomograms has been developed from the Memorial Sloan-Kettering Cancer Center that is used to predict disease progression and survival after a variety of treatments.

Morbidity and mortality

Current prostate cancer treatments, including radical prostatectomy and radiation therapy, result in permanent side effects in many men. The most common ones are erectile dysfunction and urinary incontinence.[28]

A comparison of functional outcomes in African-American versus non–African-American patients found no statistically significant difference in urinary and sexual outcomes 6 months after robotic-assisted radical prostatectomy. At 12 months, however, African-American patients had lower rates of adequate erectile function (60% vs 76.4%) and urinary continence (55.7% vs 69.8% ) compared with non–African Americans.[29]

Margel et al found that radiation therapy for prostate cancer may be associated with slightly increased risk of secondary malignancy, such as rectal cancer and bladder cancer.[30] In this study, rectal cancer occurring after radiation therapy was diagnosed at a more advanced stage and resulted in lower disease-specific survival.

Prostate cancer is the second most common cause of cancer death in males, after lung cancer. The American Cancer Society estimates that 27,540 men will die from the disease in 2015.[15]  However, in contrast with lung cancer, which accounts for 14% of new cases but 28% of cancer deaths in men, prostate cancer accounts for 26% of new cases but only 9% of deaths.[1]

Death rates from prostate cancer rose steadily from 1975 to 1991, remained level from 1991 to 1994, and have decreased since then.[1] Although this decrease has been dismissed as an artifact of lead-time bias, earlier diagnosis of progressive disease and improvements in the treatment of advanced disease are the most likely driving force behind the mortality reduction.

In the United States from 2004 to 2010, 5-year relative survival rates were greater than 99% in men with local or regional prostate cancer at diagnosis. In men with distant disease, however, survival was only 28%.[1]


Patient Education

With the advent of PSA screening, and in the absence of level I studies comparing the various options, a greater number of men require education about prostate cancer and how it is diagnosed, staged, and treated. Such education allows patients to make informed decisions about screening and, in men diagnosed with prostate cancer, to select the most appropriate treatment. Up-to-date information is available through the National Cancer Institute and the American Cancer Society, as well as Prostate

For patient education information, see the Men's Health Center and the Cancer Center, as well as Prostate Cancer, Enlarged Prostate (Benign Prostatic Hyperplasia or BPH), and Cancer: What You Need to Know.

Contributor Information and Disclosures

Gerald W Chodak, MD Editor,; Medscape Urology, Experts and Viewpoints--Controversies in Urology; Director of Medical Content, Answers Media, LLC; Author, Winning the Battle Against Prostate Cancer

Gerald W Chodak, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.


Tracey L Krupski, MD, MPH Assistant Professor, Department of Urology, University of Virginia School of Medicine

Tracey L Krupski, MD, MPH is a member of the following medical societies: American Medical Association, American Urological Association, American Society of Clinical Oncology, Society of Women in Urology

Disclosure: Nothing to disclose.

Chief Editor

Edward David Kim, MD, FACS Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center

Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, Tennessee Medical Association, Sexual Medicine Society of North America, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Repros.


Isamettin Andrew Aral, MD, MSc Attending Physician, Nassau Radiologic Group (Long Island Radiation Therapy); Clinical Assistant Professor of Radiation Oncology, State University of New York Downstate College of Medicine

Isamettin Andrew Aral, MD, MSc, is a member of the following medical societies: American College of Radiology, American Medical Association, and American Society for Therapeutic Radiology and Oncology

Disclosure: Nothing to disclose.

Hassan Aziz, MD Clinical Professor, Department of Radiation Oncology, Downstate Medical Center and Long Island College Hospital, State University of New York at Downstate

Hassan Aziz, MD is a member of the following medical societies: American College of Radiology and American Society for Therapeutic Radiology and Oncology

Disclosure: Nothing to disclose.

Michael Giasullo, MD Clinical Assistant Professor, Department of Urology, State University of New York Downstate Medical Center; Chief, Department of Surgery, Division of Urology, Lutheran Medical Center; Consulting Staff, Bay Ridge Urology Associates; Assistant Attending Physician, Department of Surgery, Urology Section, Methodist Hospital

Michael Giasullo, MD is a member of the following medical societies: American Medical Association and American Urological Association

Disclosure: Nothing to disclose.

Leonard Gabriel Gomella, MD, FACS The Bernard W Godwin Professor of Prostate Cancer Chairman, Department of Urology, Associate Director of Clinical Affairs, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Leonard Gabriel Gomella, MD, FACS is a member of the following medical societies: American Association for Cancer Research, American College of Surgeons, American Medical Association, American Society for Laser Medicine and Surgery, American Urological Association, Sigma Xi, Society for Basic Urologic Research, Society of University Urologists, and Society of Urologic Oncology

Disclosure: GSK Consulting fee Consulting; Astra Zeneca Honoraria Speaking and teaching; Watson Pharmaceuticals Consulting fee Consulting

Fazal Hussain, MD, MBBS Director, Clinical Research, King Faisal Cancer Centre

Fazal Hussain, MD, MBBS is a member of the following medical societies: American College of Radiology

Disclosure: Nothing to disclose.

Nicholas Karanikolas, MD Associate Professor, Department of Urology, SUNY Downstate College of Medicine; Director, Urologic Oncology, Staten Island University Hospital; Attending Physician, Department of Urology, Brooklyn Veterans Administration Hospital

Nicholas Karanikolas, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Dan Theodorescu, MD, PhD Paul A Bunn Professor of Cancer Research, Professor of Surgery and Pharmacology, Director, University of Colorado Comprehensive Cancer Center

Dan Theodorescu, MD, PhD is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Urological Association, Medical Society of Virginia, Society for Basic Urologic Research, and Society of Urologic Oncology

Disclosure: Key Genomics Ownership interest Co-Founder-50% Stock Ownership; KromaTiD, Inc Stock Options Board membership

  1. American Cancer Society. Cancer Facts & Figures 2015. Available at Accessed: August 6, 2015.

  2. Wolf AM, Wender RC, Etzioni RB, Thompson IM, et al. American Cancer Society guideline for the early detection of prostate cancer: update 2010. CA Cancer J Clin. 2010 Mar-Apr. 60(2):70-98. [Medline].

  3. [Guideline] Screening for Prostate Cancer: Current Recommendation. US Preventive Services Task Force. May 2012. U.S. Preventive Services Task Force. Available at Accessed: August 7, 2015.

  4. American Urological Association. AUA Disputes Panel’s Recommendations on Prostate Cancer Screening. May 21, 2012. Available at Accessed: Jan 27 2013.

  5. Hayes JH, Ollendorf DA, Pearson SD, Barry MJ, et al. Active surveillance compared with initial treatment for men with low-risk prostate cancer: a decision analysis. JAMA. 2010 Dec 1. 304(21):2373-80. [Medline]. [Full Text].

  6. Al Olama AA, Kote-Jarai Z, Giles GG, Guy M, Morrison J, et al. Multiple loci on 8q24 associated with prostate cancer susceptibility. Nat Genet. 2009 Oct. 41(10):1058-60. [Medline].

  7. Ewing CM, Ray AM, Lange EM, Zuhlke KA, Robbins CM, et al. Germline mutations in HOXB13 and prostate-cancer risk. N Engl J Med. 2012 Jan 12. 366(2):141-9. [Medline].

  8. Harding A. Prostate Cancer Risk Doubled for Men With Lynch Syndrome. Medscape Medical News. Available at Accessed: May 2, 2013.

  9. Raymond VM, Mukherjee B, Wang F, Huang SC, Stoffel EM, Kastrinos F, et al. Elevated Risk of Prostate Cancer Among Men With Lynch Syndrome. J Clin Oncol. 2013 Mar 25. [Medline].

  10. Hsing AW, Comstock GW. Serological precursors of cancer: serum hormones and risk of subsequent prostate cancer. Cancer Epidemiol Biomarkers Prev. 1993 Jan-Feb. 2(1):27-32. [Medline].

  11. Thompson IM, Goodman PJ, Tangen CM, Lucia MS, Miller GJ, Ford LG, et al. The influence of finasteride on the development of prostate cancer. N Engl J Med. 2003 Jul 17. 349(3):215-24. [Medline].

  12. Andriole GL, Bostwick DG, Brawley OW, Gomella LG, et al. Effect of dutasteride on the risk of prostate cancer. N Engl J Med. 2010 Apr 1. 362(13):1192-202. [Medline].

  13. ASCO/AUA Special Announcement on FDA Decision Re: Dutasteride. February 2, 2011. [Full Text].

  14. FDA Drug Safety Communication: 5-alpha reductase inhibitors (5-ARIs) may increase the risk of a more serious form of prostate cancer. US Food and Drug Administration. Available at Accessed: October 22, 2012.

  15. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2015. CA Cancer J Clin. 2015 Jan-Feb. 65 (1):5-29. [Medline].

  16. Fowler JE Jr, Sanders J, Bigler SA, Rigdon J, Kilambi NK, Land SA. Percent free prostate specific antigen and cancer detection in black and white men with total prostate specific antigen 2.5 to 9.9 ng./ml. J Urol. 2000 May. 163(5):1467-70. [Medline].

  17. Eggener SE, Scardino PT, Walsh PC, Han M, et al. Predicting 15-year prostate cancer specific mortality after radical prostatectomy. J Urol. 2011 Mar. 185(3):869-75. [Medline].

  18. Ananthanarayanan V, Deaton RJ, Amatya A,et al. Subcellular localization of p27 and prostate cancer recurrence: automated digital microscopy analysis of tissue microarrays. Hum Pathol. 2011 Jun. 42(6):873-81. [Medline]. [Full Text].

  19. Laidman J. Lower Mortality Associated With Opioid-Sparing Prostatectomy. Medscape Medical News. Dec 18 2013. [Full Text].

  20. Scavonetto F, Yeoh TY, Umbreit EC, et al. Association between neuraxial analgesia, cancer progression, and mortality after radical prostatectomy: a large, retrospective matched cohort study. Br J Anaesth. 2013 Dec 16. [Medline].

  21. Kenfield SA, Stampfer MJ, Chan JM, Giovannucci E. Smoking and prostate cancer survival and recurrence. JAMA. 2011 Jun 22. 305(24):2548-55. [Medline]. [Full Text].

  22. Joshu CE, Mondul AM, Meinhold CL, Humphreys EB, Han M, Walsh PC, et al. Cigarette smoking and prostate cancer recurrence after prostatectomy. J Natl Cancer Inst. 2011 May 18. 103(10):835-8. [Medline]. [Full Text].

  23. Mulcahy N. Men With Prostate Cancer Have Increased Risk for Melanoma. Medscape Medical News. Available at Accessed: November 12, 2013.

  24. Li WQ, Qureshi AA, Ma J, Goldstein AM, Giovannucci EL, Stampfer MJ, et al. Personal History of Prostate Cancer and Increased Risk of Incident Melanoma in the United States. J Clin Oncol. 2013 Nov 4. [Medline].

  25. Markert EK, Mizuno H, Vazquez A, Levine AJ. Molecular classification of prostate cancer using curated expression signatures. Proc Natl Acad Sci U S A. 2011 Dec 27. 108(52):21276-81. [Medline]. [Full Text].

  26. Mulcahy N. Tool Updated for Predicting Prostate Cancer Severity. Available at Accessed: January 15, 2013.

  27. Eifler JB, Feng Z, Lin BM, Partin MT, Humphreys EB, Han M, et al. An updated prostate cancer staging nomogram (Partin tables) based on cases from 2006 to 2011. BJU Int. 2013 Jan. 111(1):22-9. [Medline].

  28. National Cancer Institute. Prostate Cancer Screening (PDQ®). Available at Accessed: October 25, 2012.

  29. DeCastro GJ, Jayram G, Razmaria A, Shalhav A, Zagaja GP. Functional outcomes in African-Americans after robot-assisted radical prostatectomy. J Endourol. 2012 Aug. 26(8):1013-9. [Medline].

  30. Margel D, Baniel J, Wasserberg N, Bar-Chana M, Yossepowitch O. Radiation therapy for prostate cancer increases the risk of subsequent rectal cancer. Ann Surg. 2011 Dec. 254(6):947-50. [Medline].

  31. Wilt TJ, Brawer MK, Jones KM, Barry MJ, Aronson WJ, et al. Radical prostatectomy versus observation for localized prostate cancer. N Engl J Med. 2012 Jul 19. 367(3):203-13. [Medline]. [Full Text].

  32. American Cancer Society. American Cancer Society recommendations for prostate cancer early detection. Accessed October 25, 2012. [Full Text].

  33. [Guideline] National Comprehensive Cancer Network. Prostate Cancer Early Detection. V.1.2014. Available at Accessed: July 11, 2014.

  34. [Guideline] Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2008 Aug 5. 149(3):185-91. [Medline].

  35. Chustecka Z. AUA Issues New Guidelines on PSA Screening. Medscape Medical News. Available at Accessed: May 14, 2013.

  36. [Guideline] Qaseem A, Barry MJ, Denberg TD, Owens DK, Shekelle P. Screening for Prostate Cancer: A Guidance Statement From the Clinical Guidelines Committee of the American College of Physicians. Ann Intern Med. 2013 Apr 9. [Medline].

  37. Andriole GL, Crawford ED, Grubb RL 3rd, Buys SS, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med. 2009 Mar 26. 360(13):1310-9. [Medline]. [Full Text].

  38. Schröder FH, Hugosson J, Roobol MJ, Tammela TL, et al. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med. 2009 Mar 26. 360(13):1320-8. [Medline].

  39. Hugosson J, Carlsson S, Aus G, Bergdahl S, et al. Mortality results from the Göteborg randomised population-based prostate-cancer screening trial. Lancet Oncol. 2010 Aug. 11(8):725-32. [Medline].

  40. Holmberg L, Bill-Axelson A, Helgesen F, Salo JO, Folmerz P et al. A randomized trial comparing radical prostatectomy with watchful waiting in early prostate cancer. N Engl J Med. 2002 Sep 12. 347(11):781-9. [Medline].

  41. Bul M, van Leeuwen PJ, Zhu X, Schröder FH, Roobol MJ. Prostate cancer incidence and disease-specific survival of men with initial prostate-specific antigen less than 3.0 ng/ml who are participating in ERSPC Rotterdam. Eur Urol. 2011 Apr. 59(4):498-505. [Medline].

  42. Bul M, van Leeuwen PJ, Zhu X, Schröder FH, Roobol MJ. Prostate cancer incidence and disease-specific survival of men with initial prostate-specific antigen less than 3.0 ng/ml who are participating in ERSPC Rotterdam. Eur Urol. 2011 Apr. 59(4):498-505. [Medline].

  43. Shao YH, Albertsen PC, Roberts CB, Lin Y, Mehta AR, Stein MN, 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 Jul 26. 170(14):1256-61. [Medline].

  44. Vickers AJ, Till C, Tangen CM, Lilja H, Thompson IM. An empirical evaluation of guidelines on prostate-specific antigen velocity in prostate cancer detection. J Natl Cancer Inst. 2011 Mar 16. 103(6):462-9. [Medline]. [Full Text].

  45. Mitterberger M, Pinggera GM, Horninger W, et al. Comparison of contrast enhanced color Doppler targeted biopsy to conventional systematic biopsy: impact on Gleason score. J Urol. 2007 Aug. 178(2):464-8; discussion 468. [Medline].

  46. Cornelis F, Rigou G, Le Bras Y, et al. Real-time contrast-enhanced transrectal US-guided prostate biopsy: diagnostic accuracy in men with previously negative biopsy results and positive MR imaging findings. Radiology. 2013 Oct. 269(1):159-66. [Medline].

  47. Mulcahy N. Markers may indicate occult high-grade prostate cancer. Available at Accessed: March 6, 2013.

  48. Rosario DJ, Lane JA, Metcalfe C, Donovan JL, Doble A, et al. Short term outcomes of prostate biopsy in men tested for cancer by prostate specific antigen: prospective evaluation within ProtecT study. BMJ. 2012 Jan 9. 344:d7894. [Medline]. [Full Text].

  49. Lu-Yao GL, Albertsen PC, Moore DF, Shih W, Lin Y, et al. Outcomes of localized prostate cancer following conservative management. JAMA. 2009 Sep 16. 302(11):1202-9. [Medline]. [Full Text].

  50. King J. PET/MR detects prostate cancer recurrence. Medscape Medical News. June 20, 2013. [Full Text].

  51. Eiber M, Souvatzoglou M, Maurer T, et al. Initial experience in restaging of patients with recurrent prostate cancer: comparison of 11C-choline-PET/MR and 11C-choline-PET/CT [abstract 343]. Presented at: 2013 Annual Meeting of the Society of Nuclear Medicine and Molecular Imaging (SNMMI); June 11, 2013; Vancouver, British Columbia, Canada.

  52. [Guideline] Agency for Healthcare Research and Quality Guideline Clearinghouse. ACR Appropriateness Criteria® pretreatment staging prostate cancer. Available at Accessed: January 26, 2011.

  53. Ellis RJ, Kaminsky DA, Zhou EH, Fu P, Chen WD, Brelin A, et al. Ten-year outcomes: the clinical utility of single photon emission computed tomography/computed tomography capromab pendetide (Prostascint) in a cohort diagnosed with localized prostate cancer. Int J Radiat Oncol Biol Phys. 2011 Sep 1. 81(1):29-34. [Medline].

  54. American Joint Committee on Cancer. AJCC Staging Manual. 6th ed. New York, NY: Springer Verlag; 2002. [Full Text].

  55. Cooperberg MR, Broering JM, Carroll PR. Risk assessment for prostate cancer metastasis and mortality at the time of diagnosis. J Natl Cancer Inst. 2009 Jun 16. 101(12):878-87. [Medline]. [Full Text].

  56. Lowry F. Revamped prostate cancer risk calculator now online. Medscape Medical News. August 8, 2014. [Full Text].

  57. Thompson IM Jr, Leach RJ, Ankerst DP. Focusing PSA Testing on Detection of High-Risk Prostate Cancers by Incorporating Patient Preferences Into Decision Making. JAMA. 2014 Aug 4. [Medline].

  58. Crawford ED, Blumenstein BA. Proposed substages for metastatic prostate cancer. Urology. 1997 Dec. 50(6):1027-8. [Medline].

  59. Haese A, Epstein JI, Huland H, Partin AW. Validation of a biopsy-based pathologic algorithm for predicting lymph node metastases in patients with clinically localized prostate carcinoma. Cancer. 2002 Sep 1. 95(5):1016-21. [Medline].

  60. [Guideline] Thompson I, Thrasher JB, Aus G, Burnett AL, et al. Guideline for the management of clinically localized prostate cancer: 2007 update. J Urol. 2007 Jun. 177(6):2106-31. [Medline].

  61. National Cancer Institute. Prostate Cancer Treatment (PDQ®). Available at Accessed: January 28, 2011.

  62. Lu-Yao GL, Albertsen PC, Moore DF, Shih W, Lin Y, DiPaola RS, et al. Fifteen-Year Survival Outcomes Following Primary Androgen-Deprivation Therapy for Localized Prostate Cancer. JAMA Intern Med. 2014 Jul 14. [Medline].

  63. Bahn D, de Castro Abreu AL, Gill IS, Hung AJ, Silverman P, Gross ME, et al. Focal cryotherapy for clinically unilateral, low-intermediate risk prostate cancer in 73 men with a median follow-up of 3.7 years. Eur Urol. 2012 Jul. 62(1):55-63. [Medline].

  64. Boorjian SA, Thompson RH, Siddiqui S, Bagniewski S, Bergstralh EJ, Karnes RJ, et al. Long-term outcome after radical prostatectomy for patients with lymph node positive prostate cancer in the prostate specific antigen era. J Urol. 2007 Sep. 178(3 Pt 1):864-70; discussion 870-1. [Medline].

  65. Draisma G, Etzioni R, Tsodikov A, Mariotto A, Wever E, Gulati R, et al. Lead time and overdiagnosis in prostate-specific antigen screening: importance of methods and context. J Natl Cancer Inst. 2009 Mar 18. 101(6):374-83. [Medline]. [Full Text].

  66. [Guideline] National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology. Prostate Cancer [serial online]: Version 1.2015. Available at Accessed: September 16, 2015.

  67. Bill-Axelson A, Holmberg L, Ruutu M, Garmo H, Stark JR, Busch C, et al. Radical prostatectomy versus watchful waiting in early prostate cancer. N Engl J Med. 2011 May 5. 364(18):1708-17. [Medline].

  68. Agency for Healthcare Research and Quality. Comparative Effectiveness of Therapies for Clinically Localized Prostate Cancer. AHRQ: Agency for Healthcare Research and Quality. Available at Accessed: October 27, 2012.

  69. Agency for Healthcare Research and Quality. Treatments for Clinically Localized Prostate Cancer. Available at Accessed: October 27, 2012.

  70. Geinitz H, Thamm R, Keller M, Astner ST, Heinrich C, et al. Longitudinal study of intestinal symptoms and fecal continence in patients with conformal radiotherapy for prostate cancer. Int J Radiat Oncol Biol Phys. 2011 Apr 1. 79(5):1373-80. [Medline].

  71. Nihei K, Ogino T, Onozawa M, Murayama S, Fuji H, Murakami M, et al. Multi-institutional Phase II study of proton beam therapy for organ-confined prostate cancer focusing on the incidence of late rectal toxicities. Int J Radiat Oncol Biol Phys. 2011 Oct 1. 81(2):390-6. [Medline].

  72. Sheets NC, Goldin GH, Meyer AM, Wu Y, Chang Y, et al. Intensity-modulated radiation therapy, proton therapy, or conformal radiation therapy and morbidity and disease control in localized prostate cancer. JAMA. 2012 Apr 18. 307(15):1611-20. [Medline].

  73. Briganti A, Wiegel T, Joniau S, Cozzarini C, Bianchi M, et al. Early salvage radiation therapy does not compromise cancer control in patients with pT3N0 prostate cancer after radical prostatectomy: results of a match-controlled multi-institutional analysis. Eur Urol. 2012 Sep. 62(3):472-87. [Medline].

  74. [Guideline] Rosenthal SA, Bittner NH, Beyer DC, Demanes DJ, et al. American Society for Radiation Oncology (ASTRO) and American College of Radiology (ACR) practice guideline for the transperineal permanent brachytherapy of prostate cancer. Int J Radiat Oncol Biol Phys. 2011 Feb 1. 79(2):335-41. [Medline].

  75. D'Amico AV, Chen MH, Renshaw AA, Loffredo M, Kantoff PW. Androgen suppression and radiation vs radiation alone for prostate cancer: a randomized trial. JAMA. 2008 Jan 23. 299(3):289-95. [Medline].

  76. Jones CU, Hunt D, McGowan DG, Amin MB et al. Radiotherapy and short-term androgen deprivation for localized prostate cancer. N Engl J Med. 2011 Jul 14. 365(2):107-18. [Medline].

  77. Mulcahy N. Major Prostate Cancer Trial: Short HT Best in Middle Risk. Medscape Medical News. Sep 23 2013. [Full Text].

  78. Amling CL, Leibovich BC, Lerner SE, Bergstralh EJ, Blute ML, Myers RP, et al. Primary surgical therapy for clinical stage T3 adenocarcinoma of the prostate. Semin Urol Oncol. 1997 Nov. 15(4):215-21. [Medline].

  79. Messing EM, Manola J, Sarosdy M, Wilding G, Crawford ED, Trump D. Immediate hormonal therapy compared with observation after radical prostatectomy and pelvic lymphadenectomy in men with node-positive prostate cancer. N Engl J Med. 1999 Dec 9. 341(24):1781-8. [Medline].

  80. Bolla M, Collette L, Blank L, Warde P, Dubois JB, et al. Long-term results with immediate androgen suppression and external irradiation in patients with locally advanced prostate cancer (an EORTC study): a phase III randomised trial. Lancet. 2002 Jul 13. 360(9327):103-6. [Medline].

  81. Bolla M, de Reijke TM, Van Tienhoven G, Van den Bergh AC, et al. Duration of androgen suppression in the treatment of prostate cancer. N Engl J Med. 2009 Jun 11. 360(24):2516-27. [Medline].

  82. Bria E, Cuppone F, Giannarelli D, Milella M, et al. Does hormone treatment added to radiotherapy improve outcome in locally advanced prostate cancer?: meta-analysis of randomized trials. Cancer. 2009 Aug 1. 115(15):3446-56. [Medline].

  83. Mulcahy N. Radiotherapy Plus ADT Benefit Confirmed in High-risk Prostate Cancer. Medscape [serial online]. Available at Accessed: February 3, 2014.

  84. Freedland SJ, Humphreys EB, Mangold LA, Eisenberger M, Dorey FJ, Walsh PC, et al. Risk of prostate cancer-specific mortality following biochemical recurrence after radical prostatectomy. JAMA. 2005 Jul 27. 294(4):433-9. [Medline].

  85. Mottet N, Bellmunt J, Bolla M, Joniau S, Mason M, et al. EAU guidelines on prostate cancer. Part II: Treatment of advanced, relapsing, and castration-resistant prostate cancer. Eur Urol. 2011 Apr. 59(4):572-83. [Medline].

  86. de Vrij J, Willemsen RA, Lindholm L, Hoeben RC, et al. Adenovirus-derived vectors for prostate cancer gene therapy. Hum Gene Ther. 2010 Jul. 21(7):795-805. [Medline].

  87. Urba WJ, Nemunaitis J, Marshall F, Smith DC, Hege KM, Ma J, et al. Treatment of biochemical recurrence of prostate cancer with granulocyte-macrophage colony-stimulating factor secreting, allogeneic, cellular immunotherapy. J Urol. 2008 Nov. 180(5):2011-7; discussion 2017-8. [Medline].

  88. Murat FJ, Gelet A. Current status of high-intensity focused ultrasound for prostate cancer: technology, clinical outcomes, and future. Curr Urol Rep. 2008 Mar. 9(2):113-21. [Medline].

  89. Huggins C, Hodges CV. Studies on prostatic cancer. I. The effect of castration, estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate. Cancer Res. 1941;1:293-7.

  90. Byar DP, Corle DK. Hormone therapy for prostate cancer: results of the Veterans Administration Cooperative Urological Research Group studies. NCI Monogr. 1988. 165-70. [Medline].

  91. Crawford ED, Blumenstein BA, Goodman PJ, et al. Leuprolide with and without flutamide in advanced prostate cancer. Cancer. 1990 Sep 1. 66(5 Suppl):1039-44. [Medline].

  92. Immediate versus deferred treatment for advanced prostatic cancer: initial results of the Medical Research Council Trial. The Medical Research Council Prostate Cancer Working Party Investigators Group. Br J Urol. 1997 Feb. 79(2):235-46. [Medline].

  93. Crook JM, O'Callaghan CJ, Duncan G, Dearnaley DP, et al. Intermittent androgen suppression for rising PSA level after radiotherapy. N Engl J Med. 2012 Sep 6. 367(10):895-903. [Medline]. [Full Text].

  94. Calais da Silva FE, Bono AV, Whelan P, Brausi M, et al. Intermittent androgen deprivation for locally advanced and metastatic prostate cancer: results from a randomised phase 3 study of the South European Uroncological Group. Eur Urol. 2009 Jun. 55(6):1269-77. [Medline].

  95. Hussain M, Tangen CM, Berry DL, Higano CS, Crawford ED, Liu G, et al. Intermittent versus continuous androgen deprivation in prostate cancer. N Engl J Med. 2013 Apr 4. 368(14):1314-25. [Medline].

  96. Labrie F. Endocrine therapy of prostate cancer: optimal form and timing. J Clin Endocrinol Metab. 1995 Apr. 80(4):1066-71. [Medline].

  97. Huggins C, Hodges CV. Studies on prostatic cancer. I. The effect of castration, estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate. Cancer Res. 1941;1:293-7.

  98. Maximum androgen blockade in advanced prostate cancer: an overview of the randomised trials. Prostate Cancer Trialists' Collaborative Group. Lancet. 2000 Apr 29. 355(9214):1491-8. [Medline].

  99. Loblaw DA, Virgo KS, Nam R, Somerfield MR, Ben-Josef E, Mendelson DS, et al. Initial hormonal management of androgen-sensitive metastatic, recurrent, or progressive prostate cancer: 2006 update of an American Society of Clinical Oncology practice guideline. J Clin Oncol. 2007 Apr 20. 25(12):1596-605. [Medline].

  100. Sweeney CJ, Chen YH, Carducci M, Liu G, Jarrard DF, Eisenberger M, et al. Chemohormonal Therapy in Metastatic Hormone-Sensitive Prostate Cancer. N Engl J Med. 2015 Aug 5. 42 (9):863-6. [Medline]. [Full Text].

  101. Smith MR, Saad F, Egerdie B, Sieber PR, Tammela TL, Ke C, et al. Sarcopenia during androgen-deprivation therapy for prostate cancer. J Clin Oncol. 2012 Sep 10. 30(26):3271-6. [Medline]. [Full Text].

  102. FDA Drug Safety Communication: Update to Ongoing Safety Review of GnRH Agonists and Notification to Manufacturers of GnRH Agonists to Add New Safety Information to Labeling Regarding Increased Risk of Diabetes and Certain Cardiovascular Diseases. US Food and Drug Administration. October 20, 2010. Available at Accessed: October 30, 2012.

  103. Gillessen S, Templeton A, Marra G, Kuo YF, Valtorta E, Shahinian VB. Risk of colorectal cancer in men on long-term androgen deprivation therapy for prostate cancer. J Natl Cancer Inst. 2010 Dec 1. 102(23):1760-70. [Medline]. [Full Text].

  104. Morgans AK, Hancock ML, Barnette KG, Steiner MS, Morton RA, Smith MR. Racial differences in bone mineral density and fractures in men receiving androgen deprivation therapy for prostate cancer. J Urol. 2012 Mar. 187(3):889-93. [Medline].

  105. Mulcahy N. New Risk With ADT in Prostate Cancer: Kidney Injury. Medscape Medical News. Available at Accessed: July 23, 2013.

  106. Lapi F, Azoulay L, Niazi MT, Yin H, Benayoun S, Suissa S. Androgen deprivation therapy and risk of acute kidney injury in patients with prostate cancer. JAMA. 2013 Jul 17. 310(3):289-96. [Medline].

  107. Boonen S, Reginster JY, Kaufman JM, Lippuner K, et al. Fracture risk and zoledronic acid therapy in men with osteoporosis. N Engl J Med. 2012 Nov. 367(18):1714-23. [Medline].

  108. Smith MR, Egerdie B, Hernández Toriz N, Feldman R, et al. Denosumab in men receiving androgen-deprivation therapy for prostate cancer. N Engl J Med. 2009 Aug 20. 361(8):745-55. [Medline]. [Full Text].

  109. Roqué I Figuls M, Martinez-Zapata MJ, Scott-Brown M, Alonso-Coello P. Radioisotopes for metastatic bone pain. Cochrane Database Syst Rev. 2011 Jul 6. CD003347. [Medline].

  110. US Food and Drug Administration. FDA approves new drug for advanced prostate cancer [press release]. May 15, 2013. Available at Accessed: July 1, 2013.

  111. Chustecka Z. Xofigo (Radium-223) Approved for Prostate Cancer with Bone Mets. Medscape Medical News. Available at Accessed: June 11, 2013.

  112. Brady D, Parker CC, O'Sullivan JM. Bone-targeting radiopharmaceuticals including radium-223. Cancer J. 2013 Jan. 19(1):71-8. [Medline].

  113. Parker C, Heinrich D, O'Sullivan JM, Fossa SD, Chodacki A, et al. Overall survival benefit and safety profile of radium-223 chloride, a first-in-class alpha-pharmaceutical: Results from a phase III randomized trial (ALSYMPCA) in patients with castration-resistant prostate cancer (CRPC) with bone metastases. American Society of Clinical Oncology 2012 Genitourinary Cancers Symposium. Available at Accessed: November 1, 2012.

  114. Qi WX, Shen Z, Yao Y. Docetaxel-based therapy with or without estramustine as first-line chemotherapy for castration-resistant prostate cancer: a meta-analysis of four randomized controlled trials. J Cancer Res Clin Oncol. 2011 Dec. 137(12):1785-90. [Medline].

  115. Petrylak DP, Tangen C, Hussain M, et al. SWOG 99-16: Randomized phase III trial of docetaxel (D)/estramustine (E) versus mitoxantrone(M)/prednisone(p) in men with androgen-independent prostate cancer (AIPCA). Journal of Clinical Oncology, 2004 ASCO Annual Meeting Proceedings (Post-Meeting Edition). Vol 22, No 14S (July 15 Supplement), 2004:3. Available at Accessed: November 1, 2012.

  116. Tannock IF, de Wit R, Berry WR, Horti J, Pluzanska A, et al. Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. N Engl J Med. 2004 Oct 7. 351(15):1502-12. [Medline].

  117. Berthold DR, Pond GR, Soban F, de Wit R, Eisenberger M, Tannock IF. Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer: updated survival in the TAX 327 study. J Clin Oncol. 2008 Jan 10. 26(2):242-5. [Medline].

  118. Schumacher MC, Burkhard FC, Thalmann GN, Fleischmann A, Studer UE. Good outcome for patients with few lymph node metastases after radical retropubic prostatectomy. Eur Urol. 2008 Aug. 54(2):344-52. [Medline].

  119. Kantoff P, Higano CS, Berger ER, Shore N, Small EJ, et al. Updated survival results of the IMPACT trial of sipuleucel-T for metastatic castration-resistant prostate cancer (CRPC). American Society of Clinical Oncology 2010 Genitourinary Cancers Symposium. Available at Accessed: November 1, 2012.

  120. de Bono JS, Logothetis CJ, Molina A, Fizazi K, North S, Chu L, et al. Abiraterone and increased survival in metastatic prostate cancer. N Engl J Med. 2011 May 26. 364(21):1995-2005. [Medline]. [Full Text].

  121. Fizazi K, Scher HI, Molina A, Logothetis CJ, Chi KN, et al. Abiraterone acetate for treatment of metastatic castration-resistant prostate cancer: final overall survival analysis of the COU-AA-301 randomised, double-blind, placebo-controlled phase 3 study. Lancet Oncol. 2012 Oct. 13(10):983-92. [Medline].

  122. US Food and Drug Administration. FDA expands Zytiga’s use for late-stage prostate cancer. December 10, 2012. Available at Accessed: December 17, 2012.

  123. Scher HI, Fizazi K, Saad F, Taplin ME, Sternberg CN, et al. Increased survival with enzalutamide in prostate cancer after chemotherapy. N Engl J Med. 2012 Sep 27. 367(13):1187-97. [Medline].

  124. de Bono JS, Oudard S, Ozguroglu M, Hansen S, Machiels JP,et al. Prednisone plus cabazitaxel or mitoxantrone for metastatic castration-resistant prostate cancer progressing after docetaxel treatment: a randomised open-label trial. Lancet. 2010 Oct 2. 376(9747):1147-54. [Medline].

  125. Brooks M. FDA Grants Expanded Indication for Enzalutamide (Xtandi). Medscape Medical News. Available at Accessed: September 14, 2014.

  126. Fizazi K, Carducci M, Smith M, Damião R, Brown J, etc. Denosumab versus zoledronic acid for treatment of bone metastases in men with castration-resistant prostate cancer: a randomised, double-blind study. Lancet. 2011 Mar 5. 377(9768):813-22. [Medline]. [Full Text].

  127. Gaziano JM, Glynn RJ, Christen WG, Kurth T, Belanger C, et al. Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial. JAMA. 2009 Jan 7. 301(1):52-62. [Medline]. [Full Text].

  128. Lippman SM, Klein EA, Goodman PJ, Lucia MS, et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2009 Jan 7. 301(1):39-51. [Medline].

  129. Liu Y, Hu F, Li D, Wang F, Zhu L, Chen W, et al. Does physical activity reduce the risk of prostate cancer? A systematic review and meta-analysis. Eur Urol. 2011 Nov. 60(5):1029-44. [Medline].

  130. Kramer BS, Hagerty KL, Justman S, Somerfield MR, et al. Use of 5-alpha-reductase inhibitors for prostate cancer chemoprevention: American Society of Clinical Oncology/American Urological Association 2008 Clinical Practice Guideline. J Clin Oncol. 2009 Mar 20. 27(9):1502-16. [Medline]. [Full Text].

  131. Fleshner NE, Lucia MS, Egerdie B, Aaron L, Eure G, Nandy I, et al. Dutasteride in localised prostate cancer management: the REDEEM randomised, double-blind, placebo-controlled trial. Lancet. 2012 Mar 24. 379(9821):1103-11. [Medline].

  132. Abramowitz MC, Li T, Buyyounouski MK, Ross E, Uzzo RG, Pollack A, et al. The Phoenix definition of biochemical failure predicts for overall survival in patients with prostate cancer. Cancer. 2008 Jan 1. 112(1):55-60. [Medline].

  133. Dickinson L, Ahmed HU, Allen C, Barentsz JO, Carey B,et al. Magnetic resonance imaging for the detection, localisation, and characterisation of prostate cancer: recommendations from a European consensus meeting. Eur Urol. 2011 Apr. 59(4):477-94. [Medline].

  134. [Guideline] Laidman J. New ACS Guide for PCPs Managing Prostate Cancer Survivors. Medscape Medical News. Jun 11 2014. [Full Text].

  135. [Guideline] Bankhead C. Prostate Ca Guidelines Center on Primary Care. MedPage Today. Jun 11 2014. [Full Text].

  136. Smith MR, Saad F, et al. Denosumab and bone-metastasis-free survival in men with castration-resistant prostate cancer: results of a phase 3, randomised, placebo-controlled trial. Lancet. 2012 Jan 7. 379(9810):39-46. [Medline].

  137. Lee B, Mazar J, Aftab MN, Qi F, Shelley J, Li JL, et al. Long Noncoding RNAs as Putative Biomarkers for Prostate Cancer Detection. J Mol Diagn. 2014 Oct 1. [Medline].

  138. American Urological Association. Best Practice Policy Statement on Cryosurgery for the Treatment of Localized Prostate Cancer. American Urological Association. Available at Accessed: January 30, 2011.

  139. Chen J, Zhao Y, Li X, Sun P, Wang M, Wang R, et al. Imaging primary prostate cancer with 11C-Choline PET/CT: relation to tumour stage, Gleason score and biomarkers of biologic aggressiveness. Radiol Oncol. 2012 Sep. 46(3):179-88. [Medline]. [Full Text].

  140. Chou R, Dana T, Bougatsos C, Fu R, Blazina I, Gleitsmann K, Rugge JB. 2011 Oct. [Medline].

  141. Cooperberg MR, Broering JM, Carroll PR. Risk assessment for prostate cancer metastasis and mortality at the time of diagnosis. J Natl Cancer Inst. 2009 Jun 16. 101(12):878-87. [Medline]. [Full Text].

  142. Cooperberg MR, Vickers AJ, Broering JM, Carroll PR. Comparative risk-adjusted mortality outcomes after primary surgery, radiotherapy, or androgen-deprivation therapy for localized prostate cancer. Cancer. 2010 Nov 15. 116(22):5226-34. [Medline]. [Full Text].

  143. Lee CY, Mauro VF, Alexander KS. Visual and spectrophotometric determination of compatibility of alteplase and streptokinase with other injectable drugs. Am J Hosp Pharm. 1990 Mar. 47(3):606-8. [Medline].

  144. Nelson R. Long-term Data Show Ra-223 Safe in Advanced Prostate Cancer. Medscape Medical News. Available at Accessed: February 17, 2014.

  145. Shelley M, Wilt TJ, Coles B, Mason MD. Cryotherapy for localised prostate cancer. Cochrane Database Syst Rev. 2007 Jul 18. CD005010. [Medline].

Management of localized prostate cancer. This diagram depicts the relevant anatomy of the male pelvis and genitourinary tract.
Histologic scoring system showing the 2 most common patterns seen on the biopsy specimen, termed the Gleason score.
The standard approach for grading prostate cancer depends on a Gleason score, which is based on pathologic evaluation of a prostatectomy specimen and is commonly estimated from prostate biopsy tissue. Prostate cancer patterns are assigned a number from 1-5; the score is created by adding the most common pattern and the highest-grade patterns.
Prostate cancer. Adenocarcinoma around a small nerve (center). Courtesy of Thomas M. Wheeler, MD.
Prostate cancer. Small focus of adenocarcinoma on needle biopsy on right side of slide (normal glands on left side). Courtesy of Thomas M. Wheeler, MD.
Prostate cancer. Immunohistochemical stains showing normal basal cells (brown) in a benign gland with no basal cells in malignant glands (on right side with no brown staining). Malignant glands show increased expression of racemase (red cytoplasmic stain). Courtesy of Thomas M. Wheeler, MD.
Micrograph of high-grade prostatic intraepithelial neoplasia
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.