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cancer > breast cncer > Flashcards

breast cncer Flashcards

1
Q

incidence/death of breast cancer and why

A

incidence gone up, but mortality has fallen, due to early diagnosis, chemo/radiotherapy and hormonal therapies

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2
Q

what kind of cancer is breast cancer

A

carcinoma (epithelial)

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3
Q

DIAGRAM organisation of mammary gland

A

lumen that carries milk to nipple surrounded by 2 LAYERS of epithelial cells- luminal and myoepithelial (contract luminal cells) cells-

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4
Q

what kind of cell gives shape to the ducts

A

myoepithelial cells

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5
Q

DIAGRAM progression of normal to malignant breast

A

luminal epithelial cells proliferate to become benign- they then become either a lobular carcinoma, ductal carcinoma (most common) or medullary carcinoma

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6
Q

major method of staining for carcinoma involving estrogen receptor

A

using antibodies against human estrogen receptor (HER- carcinoma cells produce this receptor)- most breast cancers are HER POSITIVE

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7
Q

how estrogen receptor stimulated and what kind of receptor it is

A

nuclear receptor- receptor inactivated by binding to chaperone protein HSB90- estrogen goes into cytoplasm (lipid soluble), binds to receptor to remove HSB90- receptor then combines with another receptor to form a DIMER, which goes into nucleus to stimulate an oestrogen RESPONSE ELEMENT (part of DNA)= switch on genes= cell proliferation

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8
Q

genes switched on by dimer

A

progesterone receptor, cyclin D1, c-myc

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9
Q

what occurs in breast cancer

A

oestrogen receptor overexpressed in most breast cancers= excess proliferation

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10
Q

breast cancer in males and effect on treatment

A

mainly driven by androgens, so treatment involving less oestrogen/blockage not effective

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11
Q

purpose of endocrine therapies

A

often adjuvant (ie given once surgery done) to prevent any remaining tumour cells from growing

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12
Q

effects of endocrine therapy

A

inhibition of ovaries, blocking enzymes producing estrogen, or inhibiting response of estrogne

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13
Q

production of estrogen- 2 ways

A

GNRH to FSH/LH stimulates estrogen ACTH also released to adrenal gland to produce androgens, which are converted into estrogens by aromatase

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14
Q

ppl most affected by breast cancer

A

POST-menopausal women

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15
Q

ovarian ablation- how done, who for, and problem with these methods

A

either by surgery, or by radiation- in PRE-menopausal women however it’s iireversible

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16
Q

reversible method of ovarian ablation

A

GNRH AGONISTS- they overstimulate LHRH/GNRH receptor, downregulating receptors= less LH release= less estrogen

17
Q

anti-oestrogens- mechanism, main one, what stage cells stuck in

A

they block response of oestrogen by COMPETITIVELY inhibiting oestrogen receptor- structurally similar, but no efficacy, thus cell stuck in G1 main one TAMOFIXEN, but also fulvestrant

18
Q

importance of tamoxifen and main side effect

A

used in POST-menopausal women- hot flushes

19
Q

issues of post menopausal women and how tamoxifen helps, and thus what is it’s name

A

post-menopausal higher risk of osteoporosis and CVD due to less estrogen- tamoxifen is ANTAGONIST in breast, but actually estrogen AGONIST in bone and CVS, so reduces risk of these 2 problems- known as SERM (SELECTIVE ESTROGEN RECEPTOR MODULATOR)

20
Q

main risks of tamoxifen

A

embolism, potential for endometrial cancer, and cataracts

21
Q

problem with fulvestrant

A

is not a SERM, is always anti-estrogenic= increased risk of CVD/osteoporosis

22
Q

how tamoxifen can be PREVENTATIVE

A

reduces risk of Contralateral breast cancer (another breast cancer in other mammary gland)

23
Q

aromatase inhibitors

A

surpresses OESTRONE production- in adrenal gland in POST-menopausal women, androstenedione/testosteromade- this is then converted to oestrone in fatty tissue ie breast- thus breast produces less oestrone

24
Q

types of aromatase inhibitors

A

type 1 are irreversible, type 2 is reversible (competitive inhibition)

25
Q

enzyme involved in aromatase function

A

cytochrome P450

26
Q

progestins in breast cancer

A

breast cancers that are sensitive to both oestrogen AND progesterone can use this treatment- progestins are given excessively to overstimulate and downregulate receptor

27
Q

main progestin

A

megestrol acetate

28
Q

problems with breast cancer treatment

A

even though treatment is effective, relapses occurs, so many patients develop metastasis

29
Q

main risk factor of breast cancer

A

obesity (androgen conversion often occurs in fatty tissue)

30
Q

effect of public health programmes

A

less mortality as cancer caught early

31
Q

types of breast cancer

A

estrogen receptor positive and negative

32
Q

treatment for oestrogen receptor negative breast cancer

A

chemotherapy

cancer (18 decks)

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