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MCD Cancer > Prostate Cancer > Flashcards

Prostate Cancer Flashcards

1
Q

which staging system is used for prostate cancer?

A

Gleason

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2
Q

what is PSA?

A

Prostate Specific Antigen

– a kallikrein protein secreted by the epithelial cells of the prostate into the urethral duct.

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3
Q

where is PSA physiologically found normally? where is it abnormal to find?

A

normal to be found in urine

but not normal in the blood (has bypassed the basement membrane)

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4
Q

what levels of PSA in the blood indicates possible prostate cancer?

what else can increase PSA levels apart from prostatic cancer?

A

over 4ng/ml

can rise to >2000 nm/ml in aggressive metastatic disease

but other disease like inflammation can lead to increased PSA levels

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5
Q

what effect can prostatic hyperplasia have on urination?

A

restricted

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6
Q

what does the prostate depend on for growth?

A

testosterone (from testes)

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7
Q

what is the inheritance pattern of prostate cancer?

A

prostate cancers are heterogeneous
– due to both defects on proto-oncogenes and TSGs

PTEN and BRCA2 are potential TSGs involved.

  • However, there is no specific TSG or oncogene that predisposes or causes prostate cancer.

Closest relationship is with androgen-signalling pathways
– “androgen-independent” PC is very aggressive.

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8
Q

which type of PC is most aggressive?

A

androgen independent prostate cancer

becomes incurable and death follows within 7 months

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9
Q

epidemiology of PC

A

most common western male cancer
– incidence increases with age.

most common in the UK for males

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10
Q

which TSGs are possibly involved in PC?

A

PTEN and BRCA2

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11
Q

how is PC graded?

A

Gleason grading system
– two largest areas of tumour are biopsied and scored 1-5
(1 = least aggressive)

the two scores are quoted plus their sum
– e.g. 3 + 3, 6.

2-4 = low grade
5-7 = intermediate grade
8-10 = high grade.
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12
Q

what drugs are used as part of PC treatment?

A

1) Leuprolide
– LHRH super-agonist
– analogue to GnRH and agonises LH release

2) Flutamide
– a steroidal anti-androgen
– blocks the testosterone receptor on the prostate gland.

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13
Q

what effect can leuprolide, a LHRH agonist, have on testerone release?

A

this agonises LH release so much that it causes GnRH receptor down-regulation in the adenohypophysis

–>so less LH is released so less testosterone is released

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14
Q

what are the 2 methods of treating PC?

A

drugs (anti-androgenic) and surgery

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15
Q

what are the surgical options for prostate cancer (non metastatic)?

A

1) Radical prostatectomy
– when the cancer is confined to the prostate gland.

2) External beam radiotherapy and brachytherapy
(small radioactive “seeds” implanted).

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16
Q

why may a 75 year old man receive hormone therapy rather than surgery for PC?

A

risks involved with anaesthesia

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17
Q

what is the logic behind giving leuprolide and flutamide as a combination ?

A

leuprolide will decrease testosterone production

flutamide will reduce testosterone uptake by the cancerous prostate gland by blocking the receptor

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18
Q

what mechanisms contribute to the recurrence of PC despite anti-androgenic treatment?

A

1) increased receptor sensitivity
2) decreased co-receptor expression in internal signalling pathways
3) mutation of testosterone receptor on prostate so can be activated

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19
Q

how can markers of aggressive vs latent prostate cancer be detected?

A

a. Proteomics.
b. NMR.
c. cDNA microarrays
– detect unique patterns of gene expression
– e.g. EZH2 gene.

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20
Q

what are the issues with PSA testing being done above a certain age?

A
  • unnecessary stress
  • extra invasive tests
  • PSA testing is sensitive but not very specific
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21
Q

why is the PSA test not very specific?

A

there is no great link between PSA marker and disease

PSA can be raised due to:

  • prostatitis or UTIs (older people are more likely to pick up UTIs)
  • surgery/catherisation
  • cycling/trauma
  • PSA increases with age
22
Q

why does prostate cancer become androgen-INdependent?

A

the cancerous prostate being an androgen-dependent gland is given anti-androgenic treatment (inhibiting androgens) so the prostate becomes androgen independent after a few years

23
Q

how common is prostate cancer? [deaths]

A

2nd most common cause of male cancer death

lung cancer is the most common cause of death due to cancer

24
Q

what are the risk factors of prostate cancer?

A
  • age (biggest)
  • afro-carribean
  • family history
  • dietary factors (high fat, meat,alcohol)
  • occupational exposure to cadmium
25
Q

how does prostate cancer often present?

A

asymptotically

26
Q

how does lower urinary tract obstruction present?

A
  • hesitancy
  • poor stream
  • terminal dribbling
  • nocturia
  • pain when urinating
27
Q

what are the signs of metastatic spread?

A
  • bone pain (severe in malignancy)
  • cord compression
  • systemic: malaise anorexia, weight loss
  • paraneoplastic syndromes e.g. hypercalcaemia
28
Q

how can PSA be increased without cancer?

A
  • prostatitis or UTIs (older people are more likely to pick up UTIs)
  • surgery/catherisation
  • cycling/trauma
  • PSA increases with age
29
Q

what is CT/MRI used for?

A

assess extent of local invasion and lymph node involvement

done in conjunction with biopsy used for Gleason scoring

invasive biopsy is best avoided so multi-parameter MRI is used

30
Q

what is the low risk Gleason score?

A

2-4

31
Q

how is prostate cancer managed?

A
  • active observation of low grade tumours in older people
  • radical prostatectomy (benign tumour)
  • external beam radiotherapy (outside prostatic capsule)
32
Q

what are the side effects of prostatectomy?

A

incontinency and impotence

due to proximity of nerves to prostate

33
Q

what group of people would prostatectomy be the most successful? criteria for operability

A

< age of 70

PSA < 10-12 ng/ml

34
Q

when is external beam radiotherapy used instead of prostatectomy?

A

prostatectomy is used when tumour is confined to prostate

radiotherapy is used for tumour that has spread outside the prostate capsule (but other organs have not been affected)

35
Q

what are the side effects of radiotherapy?

A

impotency and incontinence

toxicity to bladder and bowel limited by computer planning

36
Q

what are the side effects of using LHRH agonists?

A

due to anti-androgenic effects:

  • osteoporosis
  • loss of libido
  • anaemia
  • muscle atrophy
  • memory loss
  • gynaecomastia
37
Q

what is the source of WEAK androgens?

A

adrenals

e.g. androstenedione

38
Q

what role may PTEN deactivation have in prostate cancer?

A

1) anti-apoptotic (PTEN ensures apoptosis occurs)

2) no antagonism of androgen signalling (PTEN is an antagonist)

39
Q

what are the clinical features of prostate cancer?

A
  • difficulty urinating

- rarer: haematuria, lower back pain

40
Q

what kind of gland is the prostate?

A

exocrine (make use of ducts)

41
Q

what does the PSA test not distinguish between?

A

metastatic cancer and benign prostatic hyperplasia

both affect the basal cell layer, epithelial layer and basement membrane

42
Q

when is Gleason scoring done?

A

after a positive PSA and digital rectal exam

43
Q

why is biopsy a poor form for diagnosis?

A
  • can underestimate or overestimate the tumour grade
  • needs repeat biopsies (very invasive)
  • not useful for predicting prognosis
44
Q

what is a strong argument AGAINST routine PSA screening in men without symptoms?

A
  • a raised PSA means further invasive tests need to be done
  • unnecessary anxiety till results
  • detected malignancy needs treatment with unpleasant side effects that reduce quality of life
  • possibility the lesion if left alone has no problems for the man during his lifetime
45
Q

when is hormone therapy used?

A

metastatic prostate cancer

46
Q

what does hormone therapy involved?

A
  • orchidectomy (remove main source of testosterone)

- LHHR analogue

47
Q

HPG axis

A
  • LHRH (hypothalamus)
  • LHRH receptor (pituitary)
  • LH (released)
  • Leydig (LH binds)
  • testosterone
48
Q

what effect does LHRH agonist have?

A

overstimulates LHRH receptor on pituitary causing it to desensitise

stops LH and testosterone production

49
Q

why are anti-androgens used alongside LHRH agonists?

A

weak androgens still produced by adrenals

50
Q

describe the relapse after hormone therapy

A
  • 13 months later there is a biochemical relapse
  • 2 years later there is a symptomatic relapse
  • androgen independence creates a very aggressive cancer
  • death within 7 months
51
Q

how does the cancer respond to low circulating androgens to become “androgen independent”?

A
  • amplifies response to low residual levels of androgens or weak androgens
  • increased levels of androgen receptors
  • increase proteins required for androgen signalling e.g co-activators
  • decreased co-repressors
  • mutation of androgen
    receptor so other ligands can activate it

MCD Cancer (17 decks)

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