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15 Cards in this Set

  • Front
  • Back
What happens in breast cancer?

What happens in prostate cancer?
-tumor suppressor gene mutations
-assessment of estrogen receptor and HER-2

-tumor suppressor gene mutations, prostate specific antigen testing (inflammation or infection may elevate PSA)
Growth of certain tumors is dependent on ... .
-estrogen or androgens
Mechanism of hormone action in the cell
-hormone diffusion
-cytoplasmic receptor binding
-nuclear entry
-gene transcription
hypothalamic-pituitary-reproduction axis
-pulsatile GnRH release (from hypothalamus)
-LH and FSH production and release (anterior pituitary)
-stimulation of ovaries or testes
-negative feedback control
Portal system
-hypothalamus produces GnRH
-enters capillary bed
-through portal vein
-exit capillaries
-stimulate anterior lobe
-Finasteride inhibits ... .
-Aromatase converts ... to ... .
-SERMs - do what?
-Androgen receptor antagonists block ...
-5-alpha-reductase (test to dihydrotest)
-test and androstenedione to estrogens
-antagonize the effect of estrogens
-activity of dihydro and test
Production of estrogen in ovaries involves ... cells and ... cells.
LH for ... cells, FSH for ... .
LH side increases ... .
FSH increases ... .
-thecal, granulosa
-thecal, granulosa
-androgen synthesis
-androgens to estrogens
Name three anti-androgens.
-used for?
-body will counteract by?
-bicalutamide, flutamide, nilutamide
-prostate cancer (combined w/GnRH agonists)
-tumor growth androgen-dependent (blocks androgen from receptor, inhibiting nuclear translocation)
-increase in LH (blocks neg. feedback)
-hot flashes, gynecomastia, impotence
-used for?
-BPH, alopecia, prostate cancer (off-label)
-blocks 5a-reductase (no dihydrotestosterone production, which has higher affinity for androgen receptor)
Name two SERMs.
Name an anti-androgen.
Tissues subject to estrogen effect?
Therapeutic mechanism in breast cancer?
-tamoxifen, toremifene
-bone, endometrium, breast

-breast cancer cells dependent on estrogens for growth
-competitive antagonist at estrogen receptor
-SERM binding to ER may act as agonist or antagonist (SERMs listed have antagonistic effect in breast, agonist effect in bone and endometrium; fulvestrant decreases ER expression
In-depth effect/moa of SERMs/anti-androgens on breast cancer cells
-bind estrogen receptor in tumor cell nucleus
-complex alters gene transcription
-insulin-like growth factor-1 receptor decreased, decreasing production of TGFa(stimulates tumor), increasing production of TGFb(inhibits tumor)
-decreased division of breast cancer cell
What is the mechanism for partial effect (partial agonist) of tamoxifen in terms of gene transcription?
-cofactors; example, both X and Y cofactors are needed from estrogen to produce multiple genes; SERM has only X cofactor, so only one gene is expressed; so only partial effect
Concerns with SERMs (3)
-increased risk of endometrial cancer and uterine sarcoma
-increased risk of thromboembolism (anti-thrombin III decrease)
-hepatic cancer in animals
Name 4 GnRH analogs.
-used for?
-histrelin, leuprolide, goserelin, triptorelin
-hormone-dependent cancers

-nonapeptide or decapeptide, continuously administered (implant or microspheres) causing decrease of LH and FSH (initial surge, then fall) resulting in decreased estrogens and androgens
Name three aromatase inhibitors.
-reversible and irreversible
-anastrozole and letrozole, exemestane
-block androgen conversion to estrogens, blocking estrogen-dependent tumor growth
-anastrozole and letrozole are reversible; exemestane is irreversible
-not completely specific for aromatase, some inhibitory activity on P450 family (ex. reduction in cortisol by letrozole)
-bone density loss (resorption), effect on serum lipid profile