• Prostate Cancer

    by  • 27/05/2013 • Oncology


    1. Most common malignancy in men – and may soon be the most frequent cause of cancer death in men.
    2. Many have metastatic disease at time of diagnosis
    3. Prostate cancer is highly sensitive to androgen ablation
    4. The incidence rises exponentially with age.
    5. PSA screening is controversial as it can be elevated due to many other factors: prostatitis, systemic viruses etc.
    6. Aetiology: most sporadic, but FH, radiation exposure and environmental pollutants have a role to play
    7. p/c: weight loss, anaemia, renal failure (=ureteric obstruction), bone pain (mets are sclerotic on XR), spinal cord compression, prostatism (=frequency, urgency, dysuria, nocturia, poor stream, hesitancy, dribbling, incomplete voiding, overflow)
      1. o Early disease is usually asymptomatic – may only be detected clinically by palpable rectal mass or indurated prostate gland. Tumour usually arises peripherally in gland given an obstructive (‘prostatism’ = lower urinary tract symptoms).
    8. Pathology:
    9. Types of prostate cancer:
      1. o Adenocarcinoma: most common, arises in acinar epithelium, in periphery of gland. Cells stain for acidic phosphatase and PSA. The ‘Gleason system’ – predicts the biological behaviour of the tumour (scored between grade I and grade V).
      2. o Rare subtypes (<2%): transitional cell carcinoma arises in the ductal epithelium (=stromal sarcomas, lymphomas, small cell carcinomas)
      3. o Many have metastatic disease by time of diagnosis and present with symptoms related to these (constitutional symptoms = weight loss, anaemia, bone pain, LNs, neurological)
    10. Staging:
      1. o Most typically mets to bones
      2. o May also spread to LNs (=pelvic/abdo) and also viscera.
    1. Clinical approach:
      1. o Ix to either confirm or rule out prostate cancer and determine if mets are present
      2. o If disease confined to prostate – local therapy with RT/radical prostatectomy may be appropriate (these tx have similar outcomes = >30% incontinence and impotence). Both thought to be better than watchful waiting
    2. Ix:
      1. o Examine under anaesthesia, with clinical staging and needle biopsy
      2. o Transrectal USS to identify small peripherally sited lesions – with sextant biopsy
      3. o Transurethral resection of the prostate (TURP) if there is prostatism (lower urinary tract symptoms)
      4. o Biochemistry: serum PSA >10IU suggests metastatic disease. Also test alkaline and acid phosphatase
      5. o Radiology: CT of abdo and pelvis may identify LNs. MRI of pelvis defines tumour and degree of local extension better if radical (curative) tx is an option. CXR and isotope bone scan for mets.
      6. o Screening: remains controversial – although DRE and PSA is effective in detecting disease
    3. Tx:
      1. o For localised prostatic carcinoma
      2. Surgery: for poorly differentiated tumours confined to prostate.
      3. Radical RT: similar survival figures to surgery. Research ongoing about using higher doses in more targeted ways or using combined RT with hormonal therapy.
      4. Brachytherapy: using radioactive palladium or iodine seeds implanted directly into prostate can be performed as an outpatient and is used for small low-grade tumours.
      5. Hormone treatment (=androgen ablation):
      6. Prostate cancer cell growth relies on androgens
      7. Interfering with this ‘signal’ slows locoregional and metastatic disease
      8. Bilateral orchidectomy or gonadotrophin-releasing hormone agonists (=goserelin or buserelin) can mediate this (as they only block pituitary driven testicular androgen production)
      9. Complete androgen blockade requires the use of a concomitant peripheral anti-androgen (=flutamide, bicalutamide, cyproterone acetate).
      10. HRT before RT can reduce the size of the prostate gland and hence reducing the RT tx volume and associated s/e’s and toxicity.
      11. Anti-androgen s/e’s include: hot flushes, weakness, impotence, and loss of libido
      12. o Metastatic prostate cancer:
      13. Widespread metastatic disease is often very responsive to hormone therapy – it is the 1st line in most cases and is associated with a considerable symptomatic improvement and clinical response.
      14. Response can be monitored closely with regular PSA readings.
      15. Patients may continue to respond to hormonal therapy for several years, but on average the disease escapes hormonal control after about 18/12
      16. RT can help palliate symptoms from either the primary or mets
      17. CT is not generally effective in prostate cancer and does not usually form part of standard therapy. Although there have been studies showing value in treating younger patients with mitozantrone and estramustine.
      1. Bone-seeking radioisotopes (=strontium) have an experimental role in patients with bony mets.
    1. Tx summary:
      1. o Prostate confined disease = watchful waitingprostatectomy and RT
      2. o Local disease = Hormonal therapy and RT
      3. o Metastatic disease = Hormone therapy (LHRH agonists, peripheral antiandrogens, orchidectomy, oestrogens), RT for bone pain, limited role for CT. 
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