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eMCD - Can > Cancer 12: Breast Cancer > Flashcards

Cancer 12: Breast Cancer Flashcards

1
Q

Describe the normal cellular organisation of the mammary gland

A
  • Breast = only organ that develops after birth
  • -> develops into fatty + glandular structure in puberty –> produce milk for neonate
  • In breast fat –> tubular network comes together at nipple

Note: ANY part of breast/mammary gland can give rise to tumours
(majority = tumour of epithelial cells - carcinoma )

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2
Q

What are the 2 layers of epithelial cells of the breast?

A
  1. Inner epithelial layer contacting lumen (luminal epithelial cells)
    - -> Have receptors (e.g. ER) – respond to hormone therapy
  2. Deeper myo-epithelial cell layer (some = vacuolated) just around luminal cells - has contact w basement membrane
    - -> Contract + push substances out of luminal cells into lumen
  • Between tubule = fatty stromal cells
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3
Q

Incidence of BREAST CANCER is rising, but mortality falling due to:

A
  • Earlier diagnosis – very important
  • availability of Chemo/radiotherapies
  • Hormonal therapies
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4
Q

What are the causes and risks of breast cancer?

A
  1. Early age of onset of menstruation (MOST IMP)
  2. Late age to menopause
  3. Age at 1st full-term pregnancy (early pregnancy is protective)
  4. Some forms of contraceptive pill (exposure to oestrogen)
  5. Hormone Replacement Therapy (^)
  6. Obesity
  7. Diet, physical activity, height, medication (Aspirin)
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5
Q

Describe the progression of normal breast –> to a malignant breast:

A
  1. Benign/carcinoma in situ - proliferation of luminal cells but myoepithelium = NOT breached (precancerous state)
  2. Lobular carcinoma – cancer tries to form tube-like structures, but fails - (behave normal)
  3. Medullary carcinoma – tumour cells have packed vesicles of hormones/peptides (abnormal)
  4. Infiltrating/invasive ductal carcinoma (IDC), many have no special type of histological structure = 80%/majority of breast cancers
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6
Q

immunohistochemical staining - using antibodies –> against human oestrogen receptor.

Oestrogen receptor grows in response to:

A

grows in response to oestrogen

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7
Q

note: 80% of breast cancers are Oestrogen receptor positive

A
  • breast cancer growth is oestrogen regulated
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8
Q

ER is overexpressed / under expressed in most breast cancers

presence of ER is indicative of a better / worse prognosis
(How is this different in male breast cancer?)

A

ER is overexpressed in most breast cancers

presence of ER is indicative of a better prognosis
HOWEVER - WORSE prognosis in M breast cancer

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9
Q

What are the major treatment methods of breast cancer?

A
  1. Surgery (primary treatment)
  2. Endocrine therapy
    - Adjuvant: given AFTER surgery
    - Neo-adjuvant: used before to shrink tumour
    - -> ovarian suppression
    - -> blocks oestrogen production by enzymatic inhibition
    - -> inhibits oestrogen responses
  3. Radiation therapy
  4. Chemotherapy
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10
Q

How does Ovarian Ablation + Suppression work?

A

Ovarian Ablation:
- surgical oophorectomy
- ovarian irradiation
( but process = irreversible –> no long able to have children)

LHRH agonist:

  • binds to LHRH receipts in pituitary –> cause receptor down regulation + suppresses LH release + inhibits ovarian function –> including oestrogen production
  • fully reversible

e.g goserlein, buserelin, leuprolide

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11
Q

What are some ways to treat post menopausal breast cancer patients?

A
  1. Aromatase inhibitors –> less oestrogen made from androgens
  2. Antioestrogens that block ER in mammary gland
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12
Q

How do anti oestrogen work as treatment for breast cancer?

A
  • Tamoxifen: acts as a competitive inhibitor of ER (nonsteroidal anti-oestrogen)
  • binds to ER –> but inhibits action of ER
    i. e Blocks stimulatory effects of oestrogen –> so cells held at G1 phase
  • Tamoxifen = used for metastatic disease in post-menopausal (1/3 of patients respond)

-

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13
Q

What are potential SE of Anti oestrogen?

such as Tamoxifen?

A
  • hot flushes
  • cataracts
  • stroke
  • DVT
  • associated with endometrial thickening / hyperplasia
  • thromboembolic episodes
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14
Q

What other effects does tamoxifen a SERM have on other systems?

a) effects on bone
b) effects on CVS

A
  • tamoxifen = SERM

has:
- Oestrogenic effects in bone –> protects post-menopausal women against osteoporosis

  • Oestrogenic effects on CVS –> lowers LDL + raises HDL –> decrease atherosclerosis risk in Females
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15
Q
  • Toremifene = structural derivative of tamoxifen w/ similar anti-estrogenic + oestrogenic effects
  • Faslodex = pure anti-oestrogen (anti-oestrogen in all tissues)
  • -> effective in controlling oestrogen-stimulated growth:
  • Raloxifene = antitumor agent in animals
    o Agonist in bone but no activity in breast/uterus
    o Used for osteoporosis in post-menopausal
A

-

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16
Q

What are the 2 different types of aromatase inhibitors

How do these aromatase inhibitors work as treatment method for breast cancer?

A
  1. Suicide Inhibitors (irreversible)
    - Initially competes w/ androstenedione/testosterone for active site
  • Enzyme then specifically acts on inhibitor –> yields reactive alkylating species –> form covalent bonds at/near active site –> enzyme irreversibly inactivated-. E.g. Exemestane:
  • Mild SEs - hot flushes, nausea, fatigue
  1. Competitive Inhibitors: e.g. Anastrozole, more commonly used (reversible)
    - Binds reversibly to active site + prevent product formation only as long as inhibitor occupies active site
  • Very effective drugs (front-line endocrine therapy)
  • Well-tolerated
17
Q

How do these progestins work as treatment method for breast cancer?

A

Give progestins –> overstimulate PR –> downregulate receptors –> tumour cells don’t respond to progesterone –> growth halted

  • Progestins used in uterine + breast cancer
18
Q

How would you screen for breast cancer?

A
  • Breast screening programmes use mammography to screen F (50-64) registered w/ GP
  • Each patient asked to attend for test once every 3 years.
19
Q

What are some important oestrogen regulated genes ?

A

PR
Cyclin D1
c - myc
TGF-a

20
Q

What are some targets of breast cancer treatment?

A

hypothalamus - peptide hormone LHRH acts on:

a) pit gland –> which releases ACTH –> has action on adrenal glands –> produce androgen –> which can be converted to oestrogen via aromatization
b) pit gland –> also releases LH + FSH –> which acts on ovary –> produce oestrogen + progesterone

21
Q

What is the problem with endocrine therapies in patients with metastatic breast cancer?

A
  • many patients w metastatic disease become resistant to endocrine therapies
22
Q

breast cancer

oestrogen +ve = tamoxifen
oestrogen -ve = chemootherapy

A

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eMCD - Can (15 decks)

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