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Pathology > Endocrine Related Cancer: Breast > Flashcards

Endocrine Related Cancer: Breast Flashcards

1
Q

where are the lobules of the breast?

A

they branch out from the nipples

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2
Q

what does each lobule have?

A

tiny hollow sacs – alveoli

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3
Q

what links the lobules?

A

ducts

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4
Q

where is adipose tissue found in the breast?

A

Space around lobules and ducts is adipose tissue, ligaments and connective tissue (stroma)

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5
Q

which is the main oestrogen type found during pregnancy?

A

estriol

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6
Q

which is the main oestrogen type found in women of child bearing age?

A

estradiol

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7
Q

what type of oestrogen is made in the body after menopause?

A

estrone

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8
Q

what is oestrogen essential for?

A

growth and function of the normal breast

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9
Q

what happens if there are supraphysiological levels of oestrogen?

A

selectively kill ER+ve cells

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10
Q

what happens if there are high levels of oestrogen?

A

High oestrogen, unless opposed by high progesterone, can cause uterine cancer

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11
Q

where does oestrogen have impact?

A
  • female reproductive system (breast/endometrium)
  • prostate (& male reproductive system)
  • bone (anabolic)
  • immune system
  • neurones
  • pancreatic beta cells
  • cardiovascular system
  • skin including melanocytes
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12
Q

what do oestrogen receptors bind?

A

17b-estradiol

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13
Q

how can oestrogen signalling occur?

A
  • Via ERa and classical ERE (slow)
  • Via ERb and classical ERE (slow)
  • Via ERa and ERa heterodimers (slow)
  • Via membrane receptors (rapid)
  • Via intracellular (ERb) and other transcription factors via AP1 sites and NOT ERE
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14
Q

how do endocrine therapies to breast cancer work?

A

All target the estrogen receptor (ER) in some way

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15
Q

which patients is tamoxifen most effective on?

A

patients who are both ER and PR positive compared to those who are just ER positive but PR negative

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16
Q

what is % of reduction in patients who are ER and PR positive?

A

53% reduction and risk of recurrence of patients who are both ER and PR positive

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17
Q

what is % of reduction in patients who are only ER positive?

A

23% reduction who are only ER positive

18
Q

what are selective oestrogen receptor modulators (SERMS)?

A

Lack the steroid structure of estrogens but possess a tertiary structure - allows them to bind to the ER

19
Q

what are the effects of SERMS

A
  • Differential ER expression in a given target tissue
  • Differential ER conformation on ligand binding
  • Differential recruitment of co-regulator proteins
20
Q

what are examples of SERMS?

A
  • Tamoxifen
    • Used to treat breast cancer since 1970s
  • Raloxifene
    • licensed by FDA 1997 - osteoporosis
21
Q

what are the SERMS in breast?

A

antiestrogen Binds to ER - incorrect conformational shape - unable to bind tissue-specific coactivators

22
Q

what SERM is found in the endometrium?

A

estrogen Binds to ER - activates estrogen regulated genes

23
Q

how do ER mediate gene transcription?

A

ER mediates gene transcription via AP-1 enhancer element & transcription factors Fos and Jun

24
Q

what are the benefits of tamoxifen?

A
  • 5 yr therapy of tamoxifen reduces the risk of recurrence and death TWICE as much as 2yr therapy
  • While taking tamoxifen 1 out of 2 recurrences and 1 out of 3 deaths are avoided by the therapy
25
Q

what is the carryover effect?

A

Tamoxifen continues to demonstrate further reductions in the chance of recurrence and death in years 5-9

26
Q

what are the cardiovascular benefits of tamoxifen?

A
  • Fewer non-cancer related deaths to cardiovascular events

- Serum LDL / cholesterol reduced

27
Q

what are the skeletal benefits of tamoxifen?

A

Significant reduction in incidence of fractures of weight bearing bones
Estrogen – acts as agonist on bone mineral density

28
Q

what are side effects of tamoxifen?

A
  • Menopausal symptoms (50 to 60%)
  • Depression –may be as high as 10%
  • Ocular toxicity reported with high doses
  • Thromboembolism –risk up to 10 times that experienced by healthy women, more common in elderly patients
  • Carcinogenesis – increase risk of endometrial cancer, hepatomas, clear cell sarcomas of the ovary
29
Q

what causes tamoxifen resistance?

A
  • ER beta phenotype
  • ERa ERb heterodimer formation
  • ER mutations
  • Her-2 receptor mediated ER down regulation (MAP kinase)
30
Q

what are aromatase inhibitors?

A

Class of drugs which prevent peripheral conversion precursor steroids to estrogen

31
Q

what do aromatase inhibitors cause?

A

selective impairment of gonadal steroidogenesis

32
Q

what are aromatase inhibitors capable of?

A

selected estrogen deprivation without impairing adrenal androgen biosynthesis

33
Q

what are the types of aromatase inhibitors?

A
  • Type 1 enzyme inactivators (steroidal)

- Type II competitive antagonists (non steroidal)

34
Q

how do aromatase inhibitors work?

A

Selectively block the aromatase enzyme by blocking the heme moiety

35
Q

what are examples of aromatase inhibitors?

A

Third-generation Exemestane (aromasin) (type 1), anastrazole (Arimidex), letrozole (Femara)

36
Q

what are side effects of aromatase inhibitors?

A
  • Hot flashes
  • Vaginal bleeding
  • Myalgia/ Arthalgia
  • Osteoporosis –give calcium supplements, Vitamin D and bisphosphonates
37
Q

what is phytoestrogens?

A

Naturally occurring compounds in plants consumed by humans

38
Q

what is the structure of phytoestrogens?

A

Diphenolic ring similar to estrogens & have estrogenic activity

39
Q

what are the 2 major classes of phytoestrogens?

A
  • isoflavones

- lignans

40
Q

what is the main source of phytoestrogens?

A

soybeans and flaxseed

41
Q

what are examples of isoflavones?

A

genistein

diadzein

42
Q

what are the effects of Phytoestrogens estrogen & antiestrogen?

A
  • May cause fertility problems (uterine hypertrophy, sexual differentiation/behavior)
  • Effective in prevention of bone loss
    Reduce cancer risk (breast, prostate, colon)
  • Enhance activation of NK cells (immune)
  • Influence lipid metabolism

Pathology (17 decks)

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