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MP421 > HORMONAL BASIS OF CANCER > Flashcards

HORMONAL BASIS OF CANCER Flashcards

1
Q

hormone indication with cancer

A

exogenous (HRT) and endogenous hormones drive cell division

the more cells divide the more chance they get for mutations

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2
Q

possible carcinogenic mechanisms of cancer

A
  • estrogen binds to receptor and sends grow signal to cell
  • estrogen directly induces cell growth pathways such as ERK, PI3K
  • estrogen metabolism makes nasty metabolites which can DNA damage
  • estrogen down regulates DNA damage repair so cancer cells continue to grow gathering more mutations
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3
Q

risk factors for breast cancer

A
  • early menarche
  • late menopause
  • post menopausal obesity
  • hormone replacement therapy
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4
Q

how could being overweight cause cancer

A
  1. fat cells make extra hormones and growth factors
  2. hormones and growth factors provoke more cell division
  3. this increases the chance of cancer cells being produced
  4. which can then continue to divide and cause a tumour
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5
Q

HRT and cancer

A

HRT slightly increases the risk of breast cancer, ovarian cancer, and sometimes womb cancer (risk is small)

HRT is an effective treatment of menopause, for most the benefits outweigh the risks

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6
Q

how to target the oestrogen receptor

A
  • reduce/block the formation of estrogens (aromatase inhibitors)
  • block estrogen interaction with ER (ER antagonists)
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7
Q

ER positive breast cancer

A
  • 75% of breast cancer are ER positive
  • these women can be treated with hormonal therapy
  • tamoxifen, anastrozole, letrozole, exemestane
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8
Q

advantages of Tamoxifen (ER antagonist)

A
  • reduces risk of ER+ breast cancer
  • more effect against invasive breast cancer
  • benefits persist when its no longer taken
  • strengthens bones
  • lowers LDL cholesterol
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9
Q

disadvantages of tamoxifen (ER antagonist)

A
  • increases risk of uterine cancer
  • increases risks of blood clots
  • causes menopause-like symptoms
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10
Q

tamoxifen vs aromatase inhibitors

A
  • AI tend to be used when tamoxifen fails - fewer s/e/?
  • tamoxifen prevents binding E to ER
  • AI prevents production of Es
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11
Q

personalised medicine - herceptin

A

Herceptin (Trastuzumab) for HER2 protein plus breast cancers

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12
Q

mechanisms of action of herceptin

A
  1. antibody dependent cell-mediated toxicity (ADCC)
  2. lysis of HER2- expressing cells through complement (C’) activation
  3. monoclonal antibody selectivity, targets the extraceullar domain of the HER2 protein
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13
Q

side effects of herceptin

A

infusion reactions (itching, flushing, nausea)
headache
abdominal pain

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14
Q

combination of chemotherapy drugs

A

FEC-T
fluorouracil (5FU)
epirubicin
cyclophosphamide
taxotere (docetaxel)

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15
Q

prostate cancer

A
  • most common cancer diagnosed, 2nd most frequent cause of death
  • in first instance, locally invasive (androgen-dependent)
  • recurring metastatic (castration-resistant) prostate cancer - incurable, prognosis is 16-18 months
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16
Q

treatment strategies for prostate cancer

A
  • all strategies coupled with active surveillance - monitoring the levels of prostate-specific antigen (PSA)
  • surgery (radical prostatectomy)
  • radiotherapy (branchytherapy)
  • chemotherapy
  • androgen depravation therapy (ADT)
17
Q

androgen depravation therapy (ADT)

A
  • AR antagonists (steroidal vs non-steroidal; e.g. chlormadinone acetate vs flutamide)
  • inhibitors of androgen synthesis e.g. abiraterone - inhibits extragonadal and intraumoral synthesis of androgens
18
Q

role of androgens in prostate cancer

A
  • prostate cells (normal and malignant) are physiologically dependent on androgens to grow, function and proliferate
  • testosterone is the primary male androgen majorly produced in the testes
  • dihydrotestosterone (DHT) is a metabolite of testosterone and is a more potent androgen
  • testosterone doesn’t cause cancer but promotes and encourages growth
19
Q

androgen deprivation can help to induce apoptosis or at the very least prevent further growth. it can be achieve in two ways:

A
  1. surgical or medical ‘castration’; stops the production of testosterone
  2. anti-androgen therapy; inhibits the action of testosterone preventing its interaction with the receptors on the prostate cancer cells
20
Q

inhibitors of androgen biosynthesis drugs

A

ketoconazole
abiraterone
TAK-700
TOK-001

21
Q

androgen receptor blockers

A

bicalutamide
nilutamide
flutamide
enzalutamide
ARN-509

22
Q

enzalutamide mechanism of action

A
  • inhibits androgens binding to AR
  • inhibits AR nuclear translocation
  • inhibits AR mediated DNA binding

MP421 (12 decks)

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