Prostate cancer

Most prostate cancers are adenocarcinomas. The prostate sits below the bladder, so benign enlargement, inflammation and cancer can produce overlapping urinary symptoms. Early cancer may cause no symptoms; a normal urinary stream does not exclude it.

Age, family history and inherited susceptibility can affect risk. Report relatives with prostate, breast, ovarian or pancreatic cancer, including their age at diagnosis. A new diagnosis does not by itself tell you whether the cancer is slow-growing or aggressive.

• PSA is a blood marker, not a stand-alone cancer diagnosis. Infection, benign enlargement and recent procedures can affect the result; trends and clinical context matter.
• MRI helps locate suspicious areas and assess local extension. A PI-RADS assessment describes imaging suspicion; it is not the Gleason grade or cancer stage.
• Biopsy establishes the tissue diagnosis and grade. Ask which areas were sampled, how much cancer was found and whether specialist pathology review would change the plan.
• Staging scans look for spread when the risk warrants it. PSMA PET can add information in appropriate settings, but every small focus needs interpretation rather than automatic treatment escalation.

Gleason patterns describe the architecture seen under the microscope. Grade Group translates these findings into five groups. Gleason 3 + 4 and 4 + 3 both total seven, but the greater amount of pattern 4 in 4 + 3 gives a different risk assessment.

Stage describes where cancer is: within or beyond the prostate, in regional nodes, or at distant sites. Risk groups for localized disease also use PSA, grade and tumor extent. A Grade Group 4 result is not the same as stage IV cancer.

Active surveillance is a structured option for suitable low-risk disease and selected other cases. It uses planned PSA assessment, clinical review and repeat imaging or biopsy as appropriate, with treatment if the disease is reclassified. It preserves the opportunity for curative treatment while avoiding unnecessary early side effects.

Watchful waiting has a different purpose: symptom-directed care when the benefits of curative treatment are unlikely to outweigh its burdens. The choice should reflect health, life expectancy and preferences, not age alone.

Surgery and radiation are established local treatments. Higher-risk disease may require combined approaches, including hormone therapy with radiation. Compare cancer control alongside urinary leakage, bowel effects, sexual function and the possibility of later treatment; a newer delivery technology does not automatically make one option superior.

A rising PSA can suggest biochemical recurrence before a scan shows a lesion. Interpretation differs after prostate removal and after radiation. Confirm the trend, treatment dates, PSA doubling time and previous pathology rather than treating a single result as proof of widespread disease.

After prostatectomy, salvage radiation may still offer meaningful disease control and is generally more effective when considered at a low PSA. A negative PET scan does not automatically rule out microscopic disease or remove the value of timely salvage treatment. The radiation field and any added hormone therapy depend on recurrence risk.

Androgen deprivation therapy (ADT) lowers testosterone and remains a treatment foundation in advanced disease. GnRH agonists, antagonists or surgery can achieve this through different routes. For many patients with metastatic hormone-sensitive cancer, adding an androgen receptor pathway inhibitor (ARPI), and sometimes chemotherapy, provides more effective control than ADT alone.

Castration-resistant disease means progression despite sufficiently suppressed testosterone, not that all hormone-related treatment must stop. Review testosterone, PSA, imaging, symptoms and prior drugs together. Recent US labels also use androgen pathway modulation-naïve or -sensitive (mAPMN/S) and -resistant (mAPMR); these correspond to the settings previously called metastatic hormone-sensitive and metastatic castration-resistant disease.

Inherited testing and tumor testing answer related but different questions. BRCA and other DNA-repair findings may affect treatment, while an inherited result can also matter for relatives. Ask whether a negative blood-based tumor test needs tissue testing, and whether a variant is pathogenic rather than of uncertain significance.

• PARP inhibitors have drug-specific gene and treatment requirements. US olaparib monotherapy covers qualifying HRR-mutated metastatic castration-resistant disease after enzalutamide or abiraterone; its combination with abiraterone and prednisone or prednisolone is restricted to qualifying BRCA-mutated disease.
• The US now also approves capivasertib with abiraterone and prednisone for adults with PTEN-deficient metastatic mAPMN/S prostate cancer, selected by an FDA-authorized test. PTEN deficiency is not interchangeable with any gene-panel alteration. Glucose, diarrhea and skin reactions require monitoring.

Testing can also identify uncommon findings relevant to immunotherapy or trials. Review the exact alteration, evidence and local label before choosing a treatment.

PSMA PET measures uptake of a prostate-cancer-associated target; it is not a hereditary gene test. Radioligand therapy uses a molecule carrying radiation to target suitable PSMA-expressing disease. Marrow reserve, kidney function, prior treatment and radiation precautions all affect suitability.

The current US Pluvicto label includes PSMA-positive metastatic mAPMN/S disease in combination with an ARPI. It also includes PSMA-positive mAPMR disease after an ARPI when delaying taxane chemotherapy is appropriate, or after prior taxane treatment. It should no longer be described simply as a treatment only after chemotherapy or only for hormone-resistant disease. PET selection must meet the label requirements.

Sipuleucel-T is a different approach: an autologous cellular immunotherapy approved in the US for asymptomatic or minimally symptomatic metastatic castration-resistant prostate cancer. It requires collection and processing of the patient's cells. It is not CAR-T and is not a rapid substitute for treatment of symptomatic progression. Availability outside its approved setting must be checked separately.

Discuss continence rehabilitation, sexual function and fertility before treatment where possible. ADT can affect muscle, bone, weight, glucose, mood and cardiovascular health. A plan may include suitable resistance and weight-bearing activity, fracture-risk assessment and management of existing heart or metabolic disease.

Follow-up uses PSA alongside symptoms and imaging when appropriate; PSA alone may not capture every form of progression. New severe back pain with weakness, numbness or bladder or bowel changes needs urgent assessment for possible spinal cord compression.

• Bring the biopsy or surgery pathology, serial PSA and testosterone results, MRI and PSMA PET images, and genetic reports.
• List hormone drugs, chemotherapy and radiation fields with dates, response and important side effects.
• Ask: What is the treatment goal? Which result changes the recommendation? What will this choice mean for daily function and future options?