Prostate Cancer — Causes, PSA Testing, Staging & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Prostate cancer is the most commonly diagnosed cancer in men in the UK, USA, and Australia, and the second most common cause of cancer death in men. There are approximately 1.4 million new cases globally each year. The prostate gland sits below the bladder, surrounding the urethra — it is responsible for producing seminal fluid. The vast majority of prostate cancers are adenocarcinomas arising from the peripheral zone of the prostate. Prostate cancer has an extraordinarily wide clinical spectrum: most prostate cancers are slow-growing (indolent) and may never cause symptoms or death within the man's natural lifespan — hence the challenge of appropriately screening and treating to avoid overdiagnosis and overtreatment of cancers that would never have caused harm; while a significant minority are aggressive, rapidly progressive, and potentially fatal if not treated promptly. The 5-year survival rate for localised prostate cancer exceeds 99%; for metastatic disease it falls to approximately 30-35%.

Age: the strongest risk factor — prostate cancer is rare under 50; incidence rises sharply after 60; median age at diagnosis is 66-70 years. Ethnicity: Black men have the highest incidence and mortality from prostate cancer (2-3x higher incidence compared to white men in the UK; possibly related to genetic factors and testosterone levels); East Asian men have the lowest incidence. Family history: a first-degree relative (father, brother) with prostate cancer doubles the lifetime risk; 3 or more affected relatives indicates hereditary prostate cancer. BRCA2 gene mutations: significantly increase prostate cancer risk (3-8x) and are associated with aggressive disease — BRCA2-mutated prostate cancers respond to PARP inhibitors (olaparib, rucaparib). BRCA1 mutations confer a smaller risk increase. Lynch syndrome (MMR gene mutations): increased risk of aggressive prostate cancer; responds to immune checkpoint inhibitors. Diet: high saturated fat diet and obesity are associated with more aggressive prostate cancer; Mediterranean diet and tomatoes (lycopene) may have modest protective effects. Exogenous oestrogen exposure does not increase risk — in fact, oestrogens are used as treatment in some scenarios.

Localised prostate cancer (most common at diagnosis): often completely asymptomatic — detected by elevated PSA on screening. When symptomatic, localised disease may cause lower urinary tract symptoms (LUTS) indistinguishable from benign prostatic hyperplasia (BPH): urinary frequency and nocturia, poor urinary stream, hesitancy, incomplete bladder emptying, and terminal dribbling. However, LUTS are far more commonly caused by benign BPH than prostate cancer. Locally advanced and metastatic disease: haematuria or haematospermia (blood in semen), pelvic pain, scrotal oedema from lymphatic obstruction. Bone metastases (most common site — predominantly osteosclerotic/blastic): bone pain (most commonly back, hip, pelvis), pathological fractures (vertebral, femoral), and spinal cord compression (back pain with rapidly progressive leg weakness, bilateral leg sensory changes, and bladder/bowel dysfunction — a urological emergency). General features of advanced cancer: weight loss, fatigue, anaemia. Incidental detection: found on TURP specimen performed for BPH treatment.

PSA (prostate-specific antigen): a serine protease produced exclusively by prostatic epithelium — elevated PSA indicates prostatic disease (not necessarily cancer). PSA above 4 ng/mL requires investigation; PSA velocity (rise over time) and PSA density (PSA per prostate volume) improve specificity. Digital rectal examination (DRE): identifies hard, irregular, or asymmetric prostate gland. Multiparametric MRI (mpMRI) — pre-biopsy MRI is now standard: identifies lesions suitable for targeted biopsy; Likert/PI-RADS score 1-5 (score 4-5 indicates highly suspicious lesion). MRI-targeted biopsy: systematic plus targeted transrectal or transperineal biopsy under local anaesthetic or general anaesthetic; transperineal approach has lower risk of sepsis. Histology: Gleason score (sum of two most common Gleason grades, 1-5) and Grade Group (GG1-GG5) — GG1 (Gleason 3+3=6) is low risk; GG5 (Gleason 9-10) is very high risk. Staging: CT chest/abdomen/pelvis (lymph node and visceral metastases); isotope bone scan (skeletal metastases — being replaced in high-risk disease by PSMA PET-CT scan, which is far more sensitive). TNM staging: T (local extent), N (lymph nodes), M (distant metastases). PSA for population screening: not currently recommended as a routine national screening programme in the UK due to overdiagnosis concerns, but individual informed decision-making is supported (NICE 2019).

Low-risk localised prostate cancer (GG1, PSA below 10, T1-T2a): active surveillance (AS) — serial PSA monitoring, repeat MRI, and repeat biopsy to detect progression before treating; avoids overtreatment of indolent cancers; recommended for most men with GG1 disease. Intermediate-risk localised (GG2-3): active treatment — radical prostatectomy (robot-assisted radical prostatectomy — RARP — the most common surgical approach; includes pelvic lymph node dissection; main side effects: erectile dysfunction 50-80% at 12 months, urinary incontinence 10-30% at 12 months) or external beam radiotherapy (EBRT — stereotactic body radiotherapy, SBRT, in 5 fractions is increasingly standard; combined with 6 months ADT for intermediate risk; side effects: bowel/urinary toxicity, sexual dysfunction). High-risk localised (GG4-5, PSA above 20, T3): radical prostatectomy or radiotherapy combined with 2-3 years of ADT (androgen deprivation therapy — gonadotropin-releasing hormone agonists/antagonists: leuprorelin, goserelin, degarelix). Metastatic hormone-sensitive prostate cancer (mHSPC): ADT is the backbone — combined with docetaxel chemotherapy (STAMPEDE trial) or abiraterone (STAMPEDE, LATITUDE), apalutamide (TITAN), darolutamide (ARASENS), or enzalutamide (ENZAMET) — triplet therapy (ADT + docetaxel + darolutamide) further improves survival. Metastatic castration-resistant prostate cancer (mCRPC): enzalutamide, abiraterone (with prednisolone), cabazitaxel, PARP inhibitors (olaparib — for BRCA1/2/ATM mutations), lutetium-177-PSMA-617 radioligand therapy (TheraP/VISION trials — significant improvement in PFS and OS). Bone protection: denosumab or zoledronic acid for patients on ADT or with bone metastases.

Metastatic spinal cord compression (MSCC — the most urgent oncological emergency; spinal metastases cause vertebral collapse compressing the cord; presents with progressive back pain, bilateral leg weakness, and bladder or bowel dysfunction; requires immediate MRI spine and emergency high-dose dexamethasone plus radiotherapy or surgical decompression within hours to prevent permanent paraplegia). Bone metastases (predominantly osteosclerotic — pelvis, lumbar spine, femur; cause severe chronic pain, pathological fractures, and hypercalcaemia — managed with bisphosphonate/denosumab, analgesia, and palliative radiotherapy). Erectile dysfunction and urinary incontinence (major treatment-related complications — radical prostatectomy causes ED in 50-80% and significant stress incontinence in 10-30% at 12 months; radiotherapy causes late bowel toxicity, radiation proctitis, and bladder contracture). ADT side effects (osteoporosis requiring DEXA monitoring and bisphosphonate or denosumab prophylaxis; metabolic syndrome; increased cardiovascular disease; anaemia; loss of muscle mass; mood changes; gynaecomastia). Biochemical recurrence (rising PSA after radical treatment — occurs in 30-40% within 10 years; requires salvage radiotherapy or systemic therapy escalation).

There is no established proven primary prevention for prostate cancer. Finasteride and dutasteride (5-alpha-reductase inhibitors) reduce prostate cancer incidence by ~25% in clinical trials but increase the proportion of high-grade cancers detected — not recommended as population prevention. Maintain healthy weight: obesity is associated with more aggressive prostate cancer and worse outcomes. Mediterranean diet, regular aerobic exercise, and avoiding excessive red meat and dairy consumption are reasonable lifestyle recommendations supported by observational data. Vitamin D deficiency is associated with more aggressive prostate cancer — maintain adequate levels. Smoking cessation: smokers with prostate cancer have worse survival outcomes. Men at high risk (Black men, those with BRCA2 mutations or strong family history) should discuss risk-adapted screening from age 40-45 with a GP or urologist. Genetic testing (BRCA1/2, Lynch syndrome MMR genes): appropriate for men with personal or family history of multiple BRCA-related cancers; findings guide screening and surveillance intensity and treatment decisions.

Seek emergency care for: new onset of severe back pain with bilateral leg weakness, numbness, or bladder or bowel dysfunction — this may represent metastatic spinal cord compression, which is an oncological emergency requiring immediate MRI spine and emergency radiotherapy or surgical decompression within hours to prevent permanent paralysis. See your GP promptly for: symptoms of urinary obstruction (inability to pass urine — acute urinary retention), haematuria (blood in urine — always requires investigation to exclude malignancy), or bone pain in a man with known or suspected prostate cancer. Men over 50 (or over 45 if Black or with a family history of prostate cancer) should have an informed discussion with their GP about the risks and benefits of PSA testing — NICE recommends providing information without actively promoting or discouraging it. An elevated PSA or suspicious DRE finding requires urgent referral to a urologist within 2 weeks.