PROSTATE CANCER: INTERPROFESSIONAL COLLABORATION AND PHARMACOLOGIC CARE
Faculty:
L. Austin Fredrickson, MD, FACP
L. Austin Fredrickson is an Associate Professor of Internal Medicine at Northeast Ohio Medical University, where he serves as core faculty and teaches diagnostics, therapeutics, clinical skills, and health humanities. He is board-certified in general internal medicine and practices rural primary care. 
Kristina (Tia) Neu, RN
Kristina (Tia) Neu is a licensed Registered Nurse and author currently developing in-service training for healthcare professionals. She is a National Board-Certified Health & Wellness and Lifestyle Medicine Coach. Her work experience includes several areas of the healthcare profession, such as psychiatric nursing, medical nursing, motivational health coaching, chronic case management, dental hygiene, cardiac technician, and surgical technician.
Liz Fredrickson, PharmD, BCPS
Liz Fredrickson, PharmD, BCPS, is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University (NEOMED) College of Pharmacy, where she is course director of the Parenteral Products and Basic Pharmaceutics Lab courses.
Pamela Sardo, PharmD, BS
Pamela Sardo, PharmD, BS, is a freelance medical writer and licensed pharmacist. She is the founder and principal at Sardo Solutions in Texas. Pam received her BS from the University of Connecticut and her PharmD from the University of Rhode Island. Pam’s career spans many years in retail, clinics, hospitals, long-term care, Veterans Affairs, and managed health care responsibilities across a broad range of therapeutic classes and disease states.
Abstract
Prostate cancer is the most frequently diagnosed cancer among men and a leading cause of cancer-related mortality. Approximately one in eight men will be diagnosed with prostate cancer during their lifetime. Despite advancements in screening and treatment, this condition remains a public health challenge due to its heterogeneity, variable progression, and disparities in outcomes across racial and socioeconomic populations. Within this continuing education activity, participants will review etiology, risk factors, staging, and diagnosis of prostate cancer. This activity will also review available treatment options, including chemotherapy, hormone therapy, immunotherapy, and emerging agents. Throughout the presentation, an emphasis will be placed on interprofessional communication and shared decision-making.
Accreditation Statements
In support of improving patient care, RxCe.com LLC is jointly accredited by the Accreditation CouncilTM for Continuing Medical Education (ACCME®), the Accreditation Council for Pharmacy Education (ACPE®), and the American Nurses Credentialing Center (ANCC®), to provide continuing education for the healthcare team.
This activity was planned by and for the healthcare team, and learners will receive 2 Interprofessional Continuing Education (IPCE) credits for learning and change.
Joint Universal Activity Number: The Joint Accreditation Universal Activity Numbers assigned to this activity are as follows:
Pharmacists: JA4008424-0000-26-032-H01-P
Pharmacy Technicians: JA4008424-0000-26-032-H01-T
Credits: 2 contact hour(s) (0.2 CEU(s)) of continuing education credit.
Credit Types:
IPCE Credits - 2 Credits
AAPA Category 1 Credit™️ - 2 Credits
AMA PRA Category 1 Credit™️ - 2 Credits
Pharmacy - 2 Credits
Type of Activity: Knowledge
Media: Computer-Based Training (i.e., online courses)
Estimated time to complete activity: 2 contact hour(s) (0.2 CEU(s)), including Activity Pre-Test, Post-Test, and Activity Evaluation.
Release Date: March 18, 2026 Expiration Date: March 18, 2029
Target Audience: This educational activity is for Physicians, Physician Assistants, Pharmacists, and Pharmacy Technicians
How to Earn Credit: From March 18, 2026, through March 18, 2029, participants must:
Read the “learning objectives” and “author and planning team disclosures;”
Take the “Educational Activity Pre-Test;”
Study the section entitled “Educational Activity;” and
Complete the Educational Activity Post-Test and Activity Evaluation. The Educational Activity Post-Test will be graded automatically. Following successful completion of the Educational Activity Post-Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)
CME Credit: Credit for this course will be uploaded to CPE Monitor® for pharmacists. Physicians may receive AMA PRA Category 1 Credit™️ and use these credits toward Maintenance of Certification (MOC) requirements. Physician Assistants may earn AAPA Category 1 CME credit, reportable through PA Portfolio. All learners shall verify their individual licensing board’s specific requirements and eligibility criteria.
Statement of Need
Prostate cancer is the most frequently diagnosed malignancy in men and a leading cause of cancer-related death, with outcomes strongly influenced by tumor biology, stage at diagnosis, and patient-specific risk factors. Healthcare professionals must understand androgen-driven carcinogenesis, Gleason/Grade Group systems, TNM staging, and genetic and lifestyle risk factors. Rapid expansion of systemic options requires the ability to compare mechanisms, indications, contraindications, toxicities, and monitoring of the various treatments. Shared decision-making enables navigation of the patient journey through the patient’s experience of pain, skeletal events, metabolic, and sexual adverse effects. Structured supportive care and value-based, optimal prostate cancer management depend on the integration of urology, oncology, primary care, nursing, psychosocial services, and pharmacy services. This activity aims to address these gaps to optimize care and integrate patient and family preferences.
Learning Objectives: Upon completion of this educational activity, participants should be able to:
Describe the pathophysiology, staging, and risk factors associated with prostate cancer
Compare and Contrast pharmacologic agents used in the treatment of prostate cancer
Identify supportive care strategies for patients undergoing treatment for prostate cancer
Describe the importance of multidisciplinary care and shared decision-making in the management of prostate cancer
Disclosures
The following individuals were involved in developing this activity: L. Austin Fredrickson, MD, FACP; Liz Fredrickson, PharmD, BCPS; Kristina (Tia) Neu, RN; and Pamela Sardo, PharmD, BS. None of the individuals involved in developing this activity has a conflict of interest or financial relationships related to the subject matter. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity.
© RxCe.com LLC 2026: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.
Educational Activity Pre-Test
What is the primary advantage of using GnRH antagonists over LHRH agonists in ADT?
Lower cost
Faster onset of action without testosterone surge
Oral administration
Better survival outcomes
Which medication requires co-administration with prednisone to prevent side effects?
Enzalutamide
Degarelix
Abiraterone
Bicalutamide
Which of the following interventions helps mitigate bone loss in patients receiving ADT?
Calcium and vitamin D supplementation
Androgen receptor inhibitors
High-protein diet
Finasteride
Educational Activity
Prostate Cancer: Interprofessional Collaboration and Pharmacologic Care
Introduction
Prostate cancer is the most frequently diagnosed cancer among men and a leading cause of cancer-related mortality.1 According to the American Cancer Society (ACS), approximately one in eight men will be diagnosed with prostate cancer during their lifetime.1 While patients with early-stage prostate cancer may remain asymptomatic, advanced disease can lead to significant morbidity, and prognosis depends largely on histologic grade, tumor size, and stage.2 Despite advancements in both screening and treatment, this condition remains a public health challenge due to its heterogeneity, variable progression, and disparities in outcomes across racial and socioeconomic populations.1,2 The management of prostate cancer can be challenging for both clinicians and patients and can be optimized by an organized, interprofessional approach to care.
Within this continuing education activity, participants will review the etiology, risk factors, staging, and diagnosis of prostate cancer. This activity will also cover available treatment options, including chemotherapy, hormone therapy, immunotherapy, and emerging agents. Throughout the presentation, an emphasis will be placed on interprofessional communication and shared decision-making.
Collaborative Care in Prostate Cancer Management
Interprofessional care is a cornerstone of prostate cancer management, especially in light of the disease's wide clinical spectrum.3 The National Comprehensive Cancer Network (NCCN) guidelines emphasize the critical role of multidisciplinary teams in delivering care that is patient-centered and aligned with evidence-based recommendations.4 Multidisciplinary teams typically include primary care providers, clinical pharmacists, urologists, oncologists, radiologists, pathologists, and supportive care professionals such as nurse navigators, social workers, and mental health providers.4 Each member contributes unique clinical insights that assist patients and their families in navigating both the complex diagnostic and therapeutic landscape of prostate cancer.4 Primary care physicians play important roles as the initial point of care, given that they can emphasize the importance of annual exams, which may decrease the likelihood of a more advanced-stage diagnosis. This collaborative model enables a more comprehensive patient assessment, helps prevent redundant diagnostics, and ensures the timely initiation of care.4
One of the key benefits of multidisciplinary team care is that it facilitates shared decision-making.4 Multidisciplinary clinics allow patients to meet with multiple specialists in a single visit, which can reduce the influence of specialty-specific bias that may occur within more siloed care models.4 For example, patients evaluated only by a urologist may be more likely to undergo surgery, whereas those seen in a multidisciplinary team setting receive balanced perspectives on all available and appropriate options, including surgery, radiation therapy, and active surveillance.4 Studies have shown that men seen in multidisciplinary settings are nearly twice as likely to be offered active surveillance for low-risk disease compared to those evaluated by a single provider (43% vs. 22%).5 This structure empowers patients to make informed choices, particularly in cases where overtreating could be more harmful than the disease itself.5
In addition to improving the quality of clinical decision-making, multidisciplinary teams have demonstrated benefits in care efficiency and patient satisfaction. For example, patients referred to dedicated Prostate Cancer Units (PCUs)—a structured form of multidisciplinary team care—experienced shorter time to diagnosis (22 vs. 33 days).3 These clinics also report high patient satisfaction scores across domains, including waiting time, comfort, and overall satisfaction.3 As healthcare systems seek to optimize outcomes and resource use, the multidisciplinary team model offers a scalable, cost-effective strategy to deliver high-quality, guideline-concordant prostate cancer care.3-5
Prostate Cancer Epidemiology and Etiology
Prostate cancer is one of the most common cancers among men in the United States (US), and factors including age, genetics, race, and lifestyle influence the development of this disease.2 It is most commonly diagnosed in men over the age of 65 (~60% of cases), with a median age at diagnosis of 66 years, and is rarely diagnosed in men under age 40.1 African American men and Caribbean men of African ancestry have the highest incidence and mortality rates, due to a combination of genetic predisposition and reduced access to early screening and treatment.1,2 An estimated 313,780 new cases and 35,770 prostate cancer deaths are projected in 2025.1,2 The death rate from prostate cancer declined by about 50% between 1993 and 2022, largely due to earlier detection and advances in treatment.1 However, this decline has slowed in recent years, likely reflecting an increase in cancers being diagnosed at more advanced stages.1
A combination of genetic, environmental, and lifestyle factors influences prostate cancer risk.2 Contributing factors may include differences in androgen receptor (AR) gene activity, specifically shorter CAG repeat sequences that are linked to increased AR activation and cancer risk.2 Family history also plays a key role, with individuals having a first-degree relative with prostate cancer facing double the risk.2 Inherited mutations in DNA repair genes such as BRCA1, BRCA2, CHEK2, MSH2, and HOXB13 are associated with aggressive disease, and genetic testing is recommended for individuals with a strong family history or high-risk disease.2 Additionally, an individual’s diet can impact risk. Research has found that adherence to a Mediterranean diet is associated with a lower risk, while high intake of red meat and dairy is correlated with an increased risk.2 Lycopene (from tomatoes) and green tea may also offer protective effects.2 Notably, smoking is not a proven risk factor for developing prostate cancer but is associated with higher mortality among those diagnosed, whereas alcohol consumption has not shown a consistent link to cancer development. Risk factors are summarized in Table 1.2
Table 1
Prostate Cancer Risk Factors2
| Factor | Possible Relationship |
|---|---|
| Probable Risk Factors | |
| Age | Over 70% of prostate cancer cases are diagnosed in men older than 65 years. |
| Race/Ethnicity | Black men in the United States have a higher incidence and mortality rate from prostate cancer compared to other racial and ethnic groups. |
| Genetic | Familial prostate cancer is inherited in an autosomal dominant pattern. Germline mutations (e.g., ATM, BRCA1/2, CHEK2, HOXB13, MSH2, PALB2) are more common in metastatic or high-risk disease than in localized/low-risk disease. Inherited polymorphisms (e.g., CAG repeat length) may enhance androgen receptor (AR) activation and increase risk. |
| Possible Risk Factors | |
| Environmental | Prostate cancer incidence varies globally. Immigrants tend to exhibit incidence rates intermediate between those in their country of origin and in their new country. |
| Occupational | Cadmium exposure is associated with an increased risk of prostate cancer. |
| Diet | The Mediterranean diet is associated with reduced risk. Diets high in red meat and saturated fats are linked to increased risk. A low intake of nutrients such as 25-dihydroxyvitamin D, lycopene, and β-carotene may increase the risk. |
Pathophysiology
Prostate cancer often originates in the acinar cells of the prostate gland. The majority are adenocarcinomas, which account for more than 95% of all cases.2 These cancerous cells alter the normal structure of the prostate and can vary in how aggressive they are.2 Clinicians assess this using the Gleason scoring system, which helps determine prognosis based on how similar the cancer cells look compared to normal prostate tissue.2
Prostate cancer spreads through several routes described in the following list:2
Directly into nearby tissues
Through the lymphatic system to the lymph nodes
Through the bloodstream to distant sites, most commonly bones such as the spine, pelvis, and ribs
Visceral organs, such as the liver, lungs, and brain, can also be affected, although this typically occurs later in the disease progression.2 Testosterone and dihydrotestosterone (DHT) play key roles in the development of prostate cancer.2 Dihydrotestosterone binds to androgen receptors (ARs) in prostate cells and stimulates cell growth.2 This androgen activity is regulated by a feedback loop involving the hypothalamus, pituitary gland, testes, and adrenal glands.2 In early stages, prostate cancer is typically androgen-dependent, meaning the cancer cells need testosterone to grow.2 Androgen deprivation therapy (ADT) can slow or shrink the tumor.2
Screening and Prevention
Prostate cancer screening is not recommended for all individuals; instead, it should be based on an informed discussion between the patient and provider about the potential risks and benefits.2 The goal of screening is to detect potentially curable cancers early enough to reduce mortality.2 Because prostate cancer screening is a nuanced part of preventive care, clinicians need to consider the potential harms of overdiagnosis and overtreatment. Two primary tools, prostate-specific antigen (PSA) testing and digital rectal examination (DRE), are used for screening, and each one has its limitations.2,6-8 Prostate-specific antigen is a prostate-specific but not cancer-specific marker, and its levels can be elevated due to benign prostatic hyperplasia (BPH), prostatitis, recent ejaculation, or medical procedures like catheterization or biopsy.2,6-8 Additionally, medications such as 5-alpha-reductase inhibitors can lower PSA levels by about 50%, necessitating adjusted interpretation of results.2,4 Digital rectal examination can detect asymmetries or nodules, but it has limited sensitivity and specificity, with only 25–50% of abnormalities ultimately diagnosed as cancer.2,4
Numerous major organizations, including the American Cancer Society (ACS), the U.S. Preventive Services Task Force (USPSTF) (Table 2), and the American Urological Association (AUA) (Table 3), advocate for an individualized, shared decision-making approach.6-8 Clinicians should ensure screening is discussed in the context of a patient’s age, race, family history, life expectancy, and personal values.6-8 Routine screening is generally not recommended for men with a life expectancy of less than 10 years or those over age 70 unless in excellent health.6-8
Table 2
USPTF Screening Recommendations7
| Population | Recommendation |
| Men aged 55 to 69 years | Ages 55–69: PSA-based prostate cancer screening should be an individual decision. Shared decision-making is key: Men should discuss the potential benefits and risks with their clinician before deciding. Potential benefit: Slight reduction in the risk of dying from prostate cancer. Do not screen men who do not want to be screened or express no preference. |
| Men 70 years and older | Recommends against PSA-based screening for prostate cancer in men 70 years and older |
Table 3
AUA Screening Recommendations6
| Age Group / Risk Category | Recommendation | Rationale |
| <40 years | Do not screen | Very low prevalence of clinically significant prostate cancer No benefit and potential harms |
| 40–54 years (average risk) | Do not screen routinely | Limited benefit Harms outweigh potential gains |
| 40–54 years (higher risk) | Individualized decision-making recommended | Screening may be considered in men with a significant family history or African American ancestry |
| 55–69 years | Shared decision-making is strongly recommended | Evidence supports the benefit in reducing metastasis and mortality; balance with potential harms |
| Screening Interval (for men choosing to screen) | Use ≥2-year intervals instead of annual screening | Longer intervals reduce false positives and overdiagnosis while maintaining most benefits |
| 70+ years or life expectancy <10–15 years | Do not screen routinely | Limited benefit due to competing mortality risks and a higher chance of harm |
| 70+ years (excellent health) | May benefit from screening (individualized decision) | Consider in select & very healthy individuals |
The ACS provides guidance for initiating these conversations.8
Average risk: Begin discussion at age 50
Higher risk: African American men and those with a first-degree relative diagnosed before age 65 should begin at age 45
Highest risk: Men with multiple first-degree relatives diagnosed at a young age may begin as early as age 40
If screening is pursued, PSA testing is the primary method, with DRE performed based on clinical judgment. Follow-up intervals are typically as follows.8
Every 2 years for men with PSA <2.5 ng/mL
Annually for men with PSA ≥2.5 ng/mL
Preventive strategies for prostate cancer remain under investigation. While 5-alpha-reductase inhibitors have been shown to reduce the incidence of prostate cancer by up to 25%, they may also increase the risk of aggressive tumor development.2,9 As a result, these agents are not FDA-approved for chemoprevention. Ultimately, prostate cancer screening and prevention strategies should be viewed as a dynamic and personalized process.2 Healthcare professionals are encouraged to engage patients in ongoing conversations that reflect evolving evidence, changes in health status, and patient preferences.
Evaluation and Diagnosis
Clinical Presentation
The clinical presentation of prostate cancer varies depending on the stage of the disease. In its localized form, prostate cancer is typically asymptomatic.2 As the tumor begins to invade local tissues, patients may experience urinary symptoms including hesitancy, increased frequency, dribbling, ureteral dysfunction, and potential impotence.2 In more advanced stages of the disease, systemic symptoms can appear, including back pain, spinal cord compression, lower extremity edema, pathologic fractures, anemia, and unintentional weight loss.2 These findings reflect metastatic spread and significant disease progression.2
Staging
Accurate staging of prostate cancer is critical for guiding its management (Table 4). Staging is typically based on the TNM classification system, PSA level, and histologic grade using the Gleason score. Disease is broadly classified as localized (Stage I–II), locally advanced (Stage III), or metastatic (Stage IV).2,4 The Gleason score, now translated into Grade Groups 1 through 5, reflects tumor aggressiveness, with higher scores indicating more poorly differentiated and potentially aggressive cancers.2,4
Table 4
Prostate Cancer Staging
| Initial tests | Biopsy |
| DRE | |
| PSA level | |
| Biopsy | |
| Staging tests | Bone imaging |
| Complete blood count | |
| Gleason score on biopsy specimen | |
| Liver function tests | |
| Pelvic/abdominal imaging (mpMRI) | |
| Serum phosphatases (acid/alkaline) | |
| Additional staging tests (dependent on tumor classification, PSA, and Gleason score) | Assess the indication for germline genetic testing (family history, prognosis, stage) Consider tumor (somatic mutation testing). Estimate life expectancy Lymph node evaluation Pelvic computed tomography PMSA-targeted PET-CT imaging (e.g., Ga 68 PSMA-11 and piflufolastat F 18) |
To refine treatment decisions in clinically localized prostate cancer, the NCCN Guidelines endorse a tiered risk stratification model: very low, low, favorable intermediate, unfavorable intermediate, high, and very high risk.4 These categories incorporate clinical stage (via DRE), PSA level, Grade Group, number and percentage of positive biopsy cores, and PSA density (Table 5). The NCCN also emphasizes the usefulness of tools such as PSA kinetics, multiparametric MRI, risk calculators, and genomic testing to further individualize care.4 Imaging studies—including transrectal ultrasound-guided biopsy, CT, bone scan, and MRI—are used selectively based on risk to confirm diagnosis, evaluate disease extent, and guide therapy.4
Table 5
NCCN Risk Categories4
| Risk Category | Definition/Criteria | Typical Management Approach |
| Very Low Risk | cT1c- Grade Group 1- PSA <10 ng/mL- ≤2–3 positive cores with <50% involvement- PSA density ≤0.15 ng/mL/g | Active surveillance |
| Low Risk | Similar to very low risk, but may include slightly higher PSA density or biopsy burden | Active surveillance; definitive treatment if risk factors increase |
| Favorable Intermediate Risk | Only one intermediate-risk factor (e.g., Grade Group 2 or PSA 10–20 ng/mL)- <50% positive cores | Active surveillance may be considered in select cases |
| Unfavorable Intermediate Risk | Multiple intermediate-risk features- Grade Group 3- ≥50% core involvement | Radiation + short-term ADT or surgery |
| High / Very High Risk | Advanced features with a high likelihood of progression or metastasis | Aggressive multimodal treatment (e.g., radiation + long-term ADT and/or surgery) |
Treatment Approach
General Approach
The primary goal in managing early-stage prostate cancer is to reduce both cancer-related death and treatment-related harm.2 Treatment options include surgical removal of the prostate, radiation therapy, and conservative approaches such as active surveillance or watchful waiting.2 While surgery and radiation offer a potential cure, they may carry significant side effects, so non-interventional strategies are often considered for patients with lower-risk disease or limited life expectancy.2
The treatment strategy is guided by several factors, including cancer stage, Gleason score, presence of symptoms, and the patient's anticipated lifespan.2 Evaluating life expectancy is critical in treatment planning.11 The Charlson Comorbidity Index can be used to estimate life expectancy based on the number and severity of coexisting conditions.11 Men with low-risk, asymptomatic disease may do well with close monitoring, particularly if their life expectancy is under 10 years.2,4 For patients expected to live 10 years or more, more active interventions such as prostatectomy, external beam radiation, or brachytherapy are considered. 2,4 Importantly, surgery and radiation are generally seen as equally effective for localized disease. 2,4
In advanced prostate cancer, where cure is no longer possible, treatment aims to relieve symptoms and sustain quality of life. ADT, either through surgical castration or medications that block testosterone production, is the cornerstone of treatment in this setting, as androgens typically drive prostate cancer growth. 2,4
Localized Disease Management
For patients with localized prostate cancer, treatment selection is influenced by risk category, comorbid conditions, life expectancy, and patient values.2 Watchful waiting (WW) is generally reserved for men with limited life expectancy or low-risk disease.10 Compared to radical prostatectomy, WW may lead to higher rates of both overall and prostate cancer-specific mortality over 20 years, as well as increased metastasis and long-term urinary and erectile dysfunction.10 According to research, these mortality differences appear to be most relevant in older adults (age ≥65) and those with intermediate-risk cancer.10
Active surveillance is appropriate for patients with very low or low-risk disease who prefer to avoid the potential side effects of curative therapy.2 This strategy focuses on monitoring the disease through lab tests and imaging, reserving treatment for when symptoms develop or the cancer shows signs of progression. The main benefit is avoiding the side effects of more aggressive therapies, such as surgery or radiation.2 However, there is a potential downside—if the cancer advances, delayed treatment might be more intensive.2 Active surveillance is a more structured form of monitoring, often including regular prostate biopsies. It is typically offered to men who may still be candidates for curative treatment if the disease progresses.2 Literature suggests little to no difference in all-cause or prostate cancer mortality with active waiting compared to radical prostatectomy or external beam radiation therapy (EBRT) plus ADT over 10 years.10 Importantly, it is associated with fewer treatment-related side effects, including sexual and urinary dysfunction.10
Multiple treatment options are available for localized prostate cancer, including radical prostatectomy, EBRT, and brachytherapy.11,12 A major randomized trial found no significant differences in prostate cancer–specific mortality between these modalities at 10 years, though disease progression was more common with active surveillance.11,12 Radical prostatectomy, which involves surgical removal of the prostate and surrounding lymph nodes, offers curative intent and has a 10-year survival rate exceeding 85% in appropriately selected patients.2 Radiation therapy, including EBRT and brachytherapy, is a non-surgical alternative with comparable efficacy; however, it carries risks such as urinary incontinence, bowel dysfunction, and erectile dysfunction.2,4 Current evidence is either insufficient or lacking to make reliable conclusions about the effectiveness or safety of alternative local therapies such as cryotherapy, laser ablation, and high-intensity focused ultrasound (HIFU).10
Locally Advanced and High-Risk Disease
Patients with high-risk localized or locally advanced prostate cancer frequently benefit from a multimodal treatment approach. This may include radical prostatectomy with pelvic lymph node dissection (PLND), EBRT, and ADT.2 RP is often reserved for patients with a long life expectancy and good performance status.2 It has demonstrated high 10-year cancer-specific survival rates when combined with PLND and appropriate adjuvant or salvage therapy.2 External beam radiation therapy is another effective option, particularly for patients who are not ideal surgical candidates.2 Combining EBRT with long-term ADT—typically administered for 18 to 36 months—has shown superior outcomes in high-risk patients compared to radiation alone.4
Androgen deprivation therapy may be initiated via luteinizing hormone-releasing hormone (LHRH) agonists such as leuprolide or goserelin, or via gonadotropin-releasing hormone (GnRH) antagonists like degarelix, which avoid the initial testosterone surge associated with agonists (Table 6). Common side effects of ADT include hot flashes, fatigue, metabolic syndrome, and loss of bone density.2 In select patients with very high-risk features or node-positive disease, systemic intensification with the addition of docetaxel or abiraterone to ADT and EBRT has been associated with improved outcomes and is supported by trials such as STAMPEDE.13
Metastatic Disease Management
Metastatic prostate cancer is generally categorized as either castration-sensitive (CSPC) or castration-resistant (CRPC).2,4 In CSPC, the disease still responds to reductions in testosterone, which can be achieved by surgical orchiectomy or pharmacologic ADT.2,4 This involved medications such as leuprolide, goserelin, and degarelix. Adding docetaxel chemotherapy or novel hormonal agents such as abiraterone or enzalutamide has been shown to improve survival in metastatic CSPC.2,4
In contrast, CRPC is defined by disease progression despite achieving castrate levels of testosterone (<20 ng/dL). 2,4 Management options for CRPC include second-generation androgen receptor inhibitors (e.g., enzalutamide, darolutamide), androgen biosynthesis inhibitors (e.g., abiraterone given with prednisone), chemotherapy (e.g., docetaxel, cabazitaxel), and immunotherapy (e.g., sipuleucel-T).2,4 Symptoms, performance status, prior therapies, and presence of visceral metastases guide treatment decisions. 2,4
Bone metastases occur in most men with advanced prostate cancer. 2,4 To prevent skeletal-related events (SREs), patients should be treated with bone-modifying agents such as denosumab (a RANK ligand inhibitor) or zoledronic acid (a bisphosphonate). 2,4 These agents are associated with risks such as hypocalcemia and osteonecrosis of the jaw and require monitoring of calcium and dental health.2 A multidisciplinary approach is vital to optimizing care in metastatic prostate cancer.
Pharmacotherapy
LHRH Agonists
LHRH agonists offer a reversible form of ADT with efficacy comparable to surgery.2 This class of agents includes leuprolide and goserelin, which are available in various depot or implant formulations designed for sustained hormone suppression.2,14,15 LHRH agonists stimulate an initial surge in luteinizing hormone and testosterone before inducing receptor downregulation and suppression of testosterone production.2 Common side effects include hot flashes, reduced libido, erectile dysfunction, and injection site reactions.2,14,15 In metastatic disease, an initial testosterone surge may worsen symptoms ("tumor flare), and antiandrogens are typically co-administered during the first weeks of therapy to mitigate this effect.2
Long-term ADT with LHRH agonists is associated with reduced bone mineral density and increased fracture risk.2 Calcium and vitamin D supplementation are recommended, along with baseline and follow-up bone density assessments.2 In patients with osteoporosis or metastatic bone involvement, agents such as zoledronic acid or denosumab are indicated to reduce complications.2 Metabolic disturbances, including insulin resistance, weight gain, and increased cardiovascular risk, may also occur.2 While ADT has been linked to higher rates of diabetes and cardiovascular events, data on increased cardiovascular mortality are inconclusive.2 Routine monitoring and risk mitigation strategies are essential for patients on long-term ADT.2
GnRH Antagonists
GnRH antagonists, including degarelix and relugolix, provide rapid testosterone suppression without an initial flare.2 Degarelix is given monthly via subcutaneous injection, while relugolix is an oral agent requiring daily administration.2 Both agents achieve castrate testosterone levels within one week and do not require antiandrogens during initiation.2 Relugolix has shown lower cardiovascular event rates compared to leuprolide in patients with pre-existing heart disease.2 Common side effects of GnRH antagonists include injection site reactions, liver enzyme elevations, and hot flashes.2 Relugolix therapy does require strict adherence and awareness of potential drug interactions, particularly with agents affecting QT interval or CYP3A4 and P-glycoprotein pathways.2
Antiandrogens
First-generation antiandrogens (bicalutamide, flutamide, nilutamide) are used adjunctively with ADT to block androgen receptor activity, particularly to prevent testosterone flare.2 These agents are not effective as a monotherapy for advanced disease.2 Second-generation antiandrogens (enzalutamide, apalutamide, darolutamide) have improved potency and additional mechanisms, such as inhibition of androgen receptor nuclear translocation and DNA binding.2 They are used for nonmetastatic and metastatic castration-resistant prostate cancer (CRPC), as well as metastatic castration-sensitive prostate cancer (mCSPC).2 Enzalutamide and apalutamide may cause fatigue, hypertension, rash, and increased risk of seizures.2 Apalutamide requires TSH monitoring.2 Darolutamide has minimal central nervous system penetration and may have a lower risk of neurotoxicity and seizures.2
Table 6
Prostate Cancer Hormone Therapy Dosing2
| Drug | Usual Dose | Adverse Drug Reactions |
| Bicalutamide | 150 mg/day (locally-advanced PC) | Gynecomastia, hot flashes, diarrhea, decreased libido, breast tenderness, and LFT abnormalities |
| Flutamide | 250 mg TID (metastatic PC) | Gynecomastia, hot flashes, diarrhea, decreased libido, LFT abnormalities, and methemoglobinemia |
| Nilutamide | 300 mg/day PO for 1 month, then 150 mg/day (metastatic PC) | Gynecomastia, hot flashes, constipation, visual disturbances, interstitial pneumonitis, and alcohol intolerance |
| Apalutamide | 240 mg/day PO (metastatic, castration-sensitive) | Diarrhea, nausea, hot flashes, fatigue, rash, seizures, weight loss, and hyperthyroidism |
| Darolutamide | 600 mg BID (metastatic, CSPC or CRPC) | Fatigue, diarrhea, rash, back pain, falls, hypertension, and seizures |
| Enzalutamide | 160 mg/day PO (metastatic, CSPC or CRPC) | Diarrhea, back pain, dizziness, muscle pain, seizures, and LFT abnormalities |
| Abiraterone acetate | 1,000 mg/day PO + prednisone 5 mg daily (CSPC or CRPC) | Diarrhea, edema, hypokalemia, LFT abnormalities, hypertension, and hypertriglyceridemia |
| Goserelin | 3.6 mg SQ monthly or 10.8 mg SQ every 3 months | Hot flashes, decreased libido, gynecomastia, fatigue, weight gain, and osteoporosis |
| Leuprolide | 7.5-45 mg IM monthly | Hot flashes, decreased libido, gynecomastia, fatigue, weight gain, and osteoporosis |
| Triptorelin | 3.75 mg IM Q4weeks or 11.25 mg Q12 weeks or 22.5 mg Q24 weeks | Hot flashes, decreased libido, gynecomastia, fatigue, weight gain, and osteoporosis |
| Degarelix | 240 mg SQ loading, then 80 mg SQ Q28 days | Hot flashes, decreased libido, gynecomastia, fatigue, weight gain, and osteoporosis |
| Relugolix | 360 mg PO day 1, then 120 mg PO daily | Hot flashes, hyperglycemia, hypertriglyceridemia, musculoskeletal pain, and fatigue |
Combined Androgen Blockade (CAB)
Combined androgen blockade refers to the combination of an LHRH agonist with an antiandrogen to achieve more complete androgen suppression.2 It is primarily used in patients at high risk for tumor flare or in select cases of locally advanced disease.2 Although CAB may provide modest survival benefits, its routine use remains debated due to increased toxicity and cost.2
Abiraterone
Abiraterone acetate inhibits CYP17A1, a key enzyme in androgen biosynthesis, thereby reducing testosterone levels.2,16 It is co-administered with prednisone to counteract mineralocorticoid excess and is approved for both metastatic castration-sensitive and castration-resistant prostate cancer.2 Abiraterone has been shown to improve survival across both settings and has also shown benefit when combined with docetaxel or PARP inhibitors in specific populations.2 Liver function monitoring is necessary, and food should be avoided with the standard formulation due to increased absorption.2,16
Chemotherapy
Docetaxel is the primary chemotherapy agent for prostate cancer and has demonstrated survival benefits in both castration-sensitive and castration-resistant settings.2 Docetaxel improves survival when added to ADT in patients with high-volume mCSPC (per CHAARTED criteria), and is also a first-line option in mCRPC.2 It is typically administered every 3 weeks and may be combined with prednisone.2,17 Side effects include myelosuppression, alopecia, peripheral neuropathy, and fluid retention.2 Cabazitaxel is a taxane agent used for patients with docetaxel resistance.2,18 It is preferred after docetaxel failure, especially in patients with visceral disease or aggressive symptoms. Key toxicities include neutropenia, diarrhea, and neuropathy.2,18
Immunotherapy
Sipuleucel-T is an autologous cellular immunotherapy approved for asymptomatic or minimally symptomatic CRPC.2,19 Therapy involves leukapheresis and reinfusion of activated immune cells targeting prostatic acid phosphatase.2 While it improves overall survival modestly (~4 months), its use is limited to select patients.2 Pembrolizumab, a PD-1 inhibitor, may be used in patients with microsatellite instability-high (MSI-H), mismatch repair deficiency (dMMR), or high tumor mutational burden (TMB ≥10), though these mutations are uncommon in prostate cancer.2,20
Targeted Therapy
Poly (ADP-ribose) polymerase inhibitors (PARP inhibitors) (olaparib, rucaparib, niraparib, talazoparib) exploit defects in DNA repair mechanisms in tumors with homologous recombination repair (HRR) mutations such as BRCA1/2.2 These agents have shown benefit in metastatic CRPC, especially in BRCA-mutated tumors, either as monotherapy or in combination with androgen pathway inhibitors.2 Olaparib is now FDA-approved in combination with abiraterone for mCRPC with HRR mutations (e.g., BRCA1/2).21 Olaparib and rucaparib are associated with fatigue, anemia, nausea, and CYP3A4 interactions.2,21,22 The NCCN recommends germline and somatic testing in all mCRPC cases to guide PARP use.4
Table 7
Prostate Cancer Therapy Dosing2
| Drug | Usual Dose | Toxicities | Administration |
| Cabazitaxel | 20-25 mg/m² IV every 3 weeks | Fluid retention, constipation, mucositis, myelosuppression, hypersensitivity | IV infusion over 1 hour |
| Docetaxel | 75 mg/m² IV every 3 weeks + prednisone | Fluid retention, alopecia, mucositis, myelosuppression, hypersensitivity | IV infusion over 1 hour with corticosteroid premedication |
| Pembrolizumab | 200 mg IV q3w or 400 mg IV q6w | Fatigue, immune-mediated (e.g., diarrhea, pneumonitis, thyroiditis) | IV over 30 minutes |
| Sipuleucel-T | ≥50 million autologous CD54+ cells (activated with PAP-GM-CSF); administer doses at ~2-week intervals for a total of 3 doses | Hypersensitivity, chills, fatigue, fever, headache, myalgias | IV over 1 hour, observe 30 min post-infusion, premedicate |
| Olaparib | 300 mg PO BID | Anemia, nausea, fatigue, decreased appetite, VTE | Oral BID with or without food |
| Rucaparib | 600 mg PO BID | Fatigue, nausea, anemia, hepatotoxicity, decreased appetite | Oral BID with or without food |
| Talazoparib | 0.5 mg PO daily (+ enzalutamide) | Fatigue, nausea, appetite dysgeusia, dizziness, electrolyte imbalances, myelosuppression | Oral daily with or without food |
Shared Decision-Making in Prostate Cancer Care
Shared decision-making is a vital component of contemporary prostate cancer management and is emphasized across all stages of disease in the NCCN Guidelines.4 Because prostate cancer often presents multiple treatment pathways with similar survival outcomes but differing side effect profiles, patient engagement in treatment selection is critical.4 This is especially true in early-stage and intermediate-risk disease, where options such as active surveillance, surgery, and radiation may all be appropriate depending on individual circumstances.4
Effective shared decision-making requires clinicians to clearly explain the risks, benefits, and alternatives of each management approach while actively eliciting and incorporating the patient’s values, preferences, lifestyle, life expectancy, and comorbidities.4 For instance, patients with low-risk prostate cancer who prioritize sexual function and urinary continence may opt for active surveillance. In contrast, others who are more concerned about the psychological burden of untreated cancer may favor definitive intervention.4
Decision aids—such as visual tools, structured questionnaires, or nomograms—can facilitate the shared decision-making process.4 Studies have shown that these tools not only enhance patient knowledge and satisfaction but also improve alignment between chosen treatments and patient preferences.4 In turn, this alignment can increase adherence to recommended follow-up and minimize decisional regret.4 Ultimately, shared decision-making promotes a more patient-centered model of care, fosters trust, and helps ensure that patients are not passive recipients but active participants in their treatment journey.4
Summary
Prostate cancer is a prevalent disease that requires individualized care across a spectrum of cancer stages. While many cases remain indolent and may be safely monitored, others progress to advanced and metastatic states requiring aggressive multimodal therapy. Screening remains a nuanced issue, necessitating shared decision-making with patients. Clinicians should ensure screening is discussed in the context of a patient’s age, race, family history, life expectancy, and personal values. Effective management requires an interprofessional approach. As treatment options evolve, ongoing education is critical to ensure evidence-based, patient-centered care.
References
American Cancer Society. Key Statistics for Prostate Cancer. ACS. Updated January 2024. Accessed June 16, 2025. https://www.cancer.org/cancer/types/prostate-cancer/about/key-statistics.html
Crona DJ, Cipriani AB. Prostate cancer. In: DiPiro JT, Yee GC, Haines ST, Nolin TD, Ellingrod VL, Posey L, eds. DiPiro’s Pharmacotherapy: A Pathophysiologic Approach. 12th ed. McGraw Hill; 2023.
Sciarra A, Gentile V, Panebianco V. Multidisciplinary management of prostate cancer: how and why. Am J Clin Exp Urol. 2013;1(1):12-17.
National Comprehensive Cancer Network (NCCN). NCCN Clinical Practice Guidelines in Oncology. NCNN Guidelines. Prostate Cancer. Version 2.2024. Accessed July 13, 2025. https://www.nccn.org/guidelines/guidelines-detail?category=1&id=1459
Aizer AA, Paly JJ, Zietman AL, et al. Multidisciplinary care and pursuit of active surveillance in low-risk prostate cancer. J Clin Oncol. 2012;30(25):3071-3076. doi:10.1200/JCO.2012.42.8466
American Urological Association (AUA). Prostate Cancer: Clinically Localized Guidelines. Updated 2024. Accessed July 13, 2025. https://www.auanet.org/guidelines-and-quality/guidelines/clinically-localized-prostate-cancer-aua/astro-guideline-2022
US Preventive Services Task Force. Screening for prostate cancer: US Preventive Services Task Force recommendation statement. JAMA. 2018;319(18):1901-1913. doi:10.1001/jama.2018.3710
American Cancer Society. American Cancer Society Recommendations for Prostate Cancer Early Detection. Updated 2023. Accessed June 16, 2025. American Cancer Society. American Cancer Society Recommendations for Prostate Cancer Early Detection. Updated 2023. Accessed July 13, 2025. https://www.cancer.org/cancer/types/prostate-cancer/detection-diagnosis-staging/acs-recommendations.html
Chau CH, Figg WD. Revisiting 5α-reductase inhibitors and the risk of prostate cancer. Nat Rev Urol. 2018;15(7):400-401. doi:10.1038/s41585-018-0018-9
Cookson MS, Lowrance WT, Murad MH, Kibel AS. Castration-resistant prostate cancer: AUA guideline amendment 2018. J Urol. 2018;199(3):676-682. doi:10.1016/j.juro.2017.10.074
Brawley S, Mohan R, Nein CD. Localized Prostate Cancer: Treatment Options. Am Fam Physician. 2018;97(12):798-805.
Wolf AM, Wender RC, Etzioni RB, et al. American Cancer Society guideline for the early detection of prostate cancer: update 2010. CA Cancer J Clin. 2010;60(2):70-98. doi:10.3322/caac.20066
Parker CC, James ND, Brawley CD, et al. Radiotherapy to the primary tumour for newly diagnosed, metastatic prostate cancer (STAMPEDE): a randomised controlled phase 3 trial. Lancet. 2018;392(10162):2353-2366. doi:10.1016/S0140-6736(18)32486-3
Leuprolide. Prescribing Information. CIPLA USA INC. August 27, 2024. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1563a30b-66e0-445d-ba3e-1ccd5218133f
Goserelin. Prescribing Information. TerSera Therapeutics LLC. March 24, 2023. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=294b168b-6e5f-4db9-bf70-d599271458b3
Abiraterone. Prescribing Information. Janssen Biotech, Inc. March 28, 2025. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4e338e89-3cf2-48eb-b6e2-a06c608c6513
Docetaxel. Prescribing Information. Avyxa Pharma, LLC. July 3, 2024. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4763744e-360e-4d37-be05-cce4114548cd
Cabazitaxel. Prescribing Information. Sanofi-Aventis U.S. LLC. May 20, 2025. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=de3d9c26-572b-4ea4-9b2d-dd58a2b3e8fa
Sipuleucel-T. Prescribing Information. Dendreon Pharmaceuticals LLC. October 10, 2024. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=8309b497-5d4e-4408-ac0c-2452c11c8a35
Pembrolizumab. Prescribing Information. Merck Sharp & Dohme LLC. June 12, 2025. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9333c79b-d487-4538-a9f0-71b91a02b287
Olaparib. Prescribing Information. AstraZeneca Pharmaceuticals LP. November 6, 2023. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=741ff3e3-dc1a-45a6-84e5-2481b27131aa
Rucaparib. Prescribing Information. pharmaand GmbH. January 27, 2025. Accessed July 13, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=0295d202-1cfe-7659-e063-6294a90a476e
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