Endocrine Therapy: SERMs and SERDs Flashcards Preview

Oncology Exam 1 > Endocrine Therapy: SERMs and SERDs > Flashcards

Flashcards in Endocrine Therapy: SERMs and SERDs Deck (17)
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1
Q

Cancer Development

A

Arising from hormone-responsive tissues (breast, prostate, uterus) remain responsive to hormones and hormone receptor agonists/antagonists

2
Q

Estrogen drives and decreases

A

Drives proliferation

Decreased apoptosis

3
Q

Estrogen Synthesis

A

All estrogens come from cholesterol

Tesosterone is converted to estradiol

4
Q

Aromatase converts:

A

o Testosterone → estradiol

o Androstenedione → estrone

5
Q

Pre-Menopausal Estrogen Production

A

 Hypothalamus release GnRH to make FSH and LH which inturn goes to the ovaries
 10% of estrogen comes from peripheral tissues (adrenal gland, breast, liver, adipose tissues)(90% of estrogen gets made here)

6
Q

Post-Menopausal Estrogen Production

A

 Ovaries stops making estrogen so there is only like 10% of estrogen in the circulation from the peripheral tissues

7
Q

Premenopausal Women- Estrogen Deprivation

A

o Ovariectomy + Tamoxifen (blocked the 10% from the peripheral tissues)

8
Q

Postmenopausal Women – Estrogen Deprivation

A

Aromatase Inhibitors

9
Q

Estrogen Receptors

A

o AF1: growth factor binding domain
o AF2: Ligand binding domain
o Estrogen alpha is the most important in breast cancer and is a little larger

10
Q

Mode of Action of Estradiol

A

o Once estrogen comes in contact with the receptor it dimerizes
o AF1/2 are formed which then recruit coactivator(different transcription factors)
o It then binds to estrogen response genes
o Once they bind, they generate more and more RNA which leads to more transcription

11
Q

Selective Estrogen Receptor Modulators (SERMs) Drugs

A

 Raloxifene (evista) - Osteoporosis
 Tamoxifen (nolvadex)
 Toremifene (fareston)

12
Q

SERMs MOA

A

 Bind to estrogen receptors and acts like an antagonizers to cut of estrogen compounds

13
Q

SERMS + Breast and Uterus

A

 Binding in the breast leads to no proliferation

 Binding in the uterus leads to uterine cell proliferation

14
Q

Tamoxifen Use

A

breast cancer, chemopreventative for breast cancer

15
Q

Tamoxifen MOA

A

Binds to estrogen receptors, it causes abnormal organization of the receptor which leads to the AF2 not attaching → most of estrogen effects are lost
- AF2 regulates most of the estrogenic transcription

16
Q

Tamoxifen and Toremifiene SE

A
•	Hot flashes
•	Decreased libido
•	Tumor flare
o	Increased tumor growth that comes down
•	Vaginal Bleeding
•	Thrombosis
•	Cataracts
•	Endometrial cancer
17
Q

Fulvestrant Use and MOA

A

 Use: Metastatic breast cancer
 MOA: Binds to estrogen receptors and no matter where it has antagonistic effects → no estrogen effects (pure anti-estrogen)
- IM once monthly