PCol825B Anti-Cancer Drugs: Hormone Agonists, Antagonists, Immune
Response Modifiers, Supportive Care, Precisely Targeted Agents, and Im
mune Checkpoint Inhibitors
1. What are the ways steroid hormones act?: -A two-step mechanism where the hormone enters
the cells and binds to its cognate receptor
-The ligand-bound receptor alters gene expression to change cell growth, survival, and
phenotypic behavior
2. Are synthetic glucocorticoids agonists or antagonists of hormone path- ways?: Agonists
3. Rank the glucocorticoids used as hormone agonists in order from most potent to least:
Dexamethasone > prednisone > hydrocortisone
4. What is the MOA of glucocorticoids as hormone agonists?: Binds its specific receptor,
translocates to the cell nucleus, alters gene expression, and causes programmed cell death of
the cancer cell (apoptosis)
5. What are the indications of glucocorticoids as hormone agonists?: -Lym- phomas, multiple
myeloma, chronic and acute lymphocytic leukemia
-Brain tumors or metastases (shrinks edema around the tumor)
-In high doses blocks cortical pathways of emesis (learned response)
-Treatment of hypercalcemia associated with malignancy
6. What are the toxicities of glucocorticoids?: -Adrenal suppression
-Edema
-Electrolyte changes
-Ulcer
-Immunosuppression
-Muscle weakness
-Neurological and dermatologic toxicity
-Can exacerbate diabetes
-Excitation in high doses
7. What are progestins?: Hormone agonists that are synthetic progesterone
8. What are the MOAs of progestins?: Binds to progestin receptors (PR) which decreases
number of estrogen receptors (ER) and enhances the metabolism of estrogen
9. What are the progestins?: -Megestrol (Megace)
-Medroxyprogestone (Depo-Provera)
10.T/F: The progestins are anti-estrogenic: True
11.What are the indications for progestins?: -Endometrial carcinoma
-Breast carcinoma
-Renal cell carcinoma
12.What are the toxicities of the progestins?: -Thrombotic disorders
-Masculinization
-Depression
1/
, PCol825B Anti-Cancer Drugs: Hormone Agonists, Antagonists, Immune
Response Modifiers, Supportive Care, Precisely Targeted Agents, and Im
mune Checkpoint Inhibitors
-Amenorrhea
-Weight gain
-Fluid retention
13.What is the MOA of gonadotrophin releasing hormone agonists?: -Acts at the pituitary first to
transiently stimulate LH and FSH production and subsequently androgen production
-This transient stimulation is followed by GnRH receptor desensitization and a subsequent
decline in androgen production
-This drug can be viewed as an indirect-acting anti-androgen
14.Where do gonadotrophin releasing hormone agonists block androgen production?: -Ovaries
(decreased estrogen production)
-Testes (decreased testosterone)
15.Gonadotrophin releasing hormone agonists action has been called med- ical: Castration
16.T/F: GnRH agonists block adrenal androgen production: False, so leuprolide is often combined
with flutamide which is an androgen receptor antagonist
17.What are the indications for gonadotrophin releasing hormone agonists like leuprolide?:
Prostate cancer, primarily palliative effects
18.What are the toxicities of gonadotrophin releasing hormone agonists like leuprolide?: -Hot
flashes
-Bone pain
-Decreased libido
-CNS effects (HA, sleep disorders, etc.)
-Edema
-Hypotension
19.What are gonadotrophin releasing hormone agonists?: -Synthetic peptide derivative of
gonadotrophin-releasing hormone (GnRH); aka luteinizing hormone-re- leasing hormone (LH-RH)
-Ex/ leuprolide
20.What are the estrogen receptor antagonists/agonists known as selective estrogen receptor
modulators (SERMs)?: -Tamoxifen
-Raloxifene
-Tomremifine
21. What is the MOA of the selective estrogen receptor modulators (SERMs)?-
: -Binds to estrogen receptors (ER) in cytoplasm of breast cancer cells to block estrogen
dependent tumor cell growth in GI and therefore is cytostatic
-These agents maintain bone density (estrogen like effect) and ameliorate factors associated
with coronary heart disease
2/
Response Modifiers, Supportive Care, Precisely Targeted Agents, and Im
mune Checkpoint Inhibitors
1. What are the ways steroid hormones act?: -A two-step mechanism where the hormone enters
the cells and binds to its cognate receptor
-The ligand-bound receptor alters gene expression to change cell growth, survival, and
phenotypic behavior
2. Are synthetic glucocorticoids agonists or antagonists of hormone path- ways?: Agonists
3. Rank the glucocorticoids used as hormone agonists in order from most potent to least:
Dexamethasone > prednisone > hydrocortisone
4. What is the MOA of glucocorticoids as hormone agonists?: Binds its specific receptor,
translocates to the cell nucleus, alters gene expression, and causes programmed cell death of
the cancer cell (apoptosis)
5. What are the indications of glucocorticoids as hormone agonists?: -Lym- phomas, multiple
myeloma, chronic and acute lymphocytic leukemia
-Brain tumors or metastases (shrinks edema around the tumor)
-In high doses blocks cortical pathways of emesis (learned response)
-Treatment of hypercalcemia associated with malignancy
6. What are the toxicities of glucocorticoids?: -Adrenal suppression
-Edema
-Electrolyte changes
-Ulcer
-Immunosuppression
-Muscle weakness
-Neurological and dermatologic toxicity
-Can exacerbate diabetes
-Excitation in high doses
7. What are progestins?: Hormone agonists that are synthetic progesterone
8. What are the MOAs of progestins?: Binds to progestin receptors (PR) which decreases
number of estrogen receptors (ER) and enhances the metabolism of estrogen
9. What are the progestins?: -Megestrol (Megace)
-Medroxyprogestone (Depo-Provera)
10.T/F: The progestins are anti-estrogenic: True
11.What are the indications for progestins?: -Endometrial carcinoma
-Breast carcinoma
-Renal cell carcinoma
12.What are the toxicities of the progestins?: -Thrombotic disorders
-Masculinization
-Depression
1/
, PCol825B Anti-Cancer Drugs: Hormone Agonists, Antagonists, Immune
Response Modifiers, Supportive Care, Precisely Targeted Agents, and Im
mune Checkpoint Inhibitors
-Amenorrhea
-Weight gain
-Fluid retention
13.What is the MOA of gonadotrophin releasing hormone agonists?: -Acts at the pituitary first to
transiently stimulate LH and FSH production and subsequently androgen production
-This transient stimulation is followed by GnRH receptor desensitization and a subsequent
decline in androgen production
-This drug can be viewed as an indirect-acting anti-androgen
14.Where do gonadotrophin releasing hormone agonists block androgen production?: -Ovaries
(decreased estrogen production)
-Testes (decreased testosterone)
15.Gonadotrophin releasing hormone agonists action has been called med- ical: Castration
16.T/F: GnRH agonists block adrenal androgen production: False, so leuprolide is often combined
with flutamide which is an androgen receptor antagonist
17.What are the indications for gonadotrophin releasing hormone agonists like leuprolide?:
Prostate cancer, primarily palliative effects
18.What are the toxicities of gonadotrophin releasing hormone agonists like leuprolide?: -Hot
flashes
-Bone pain
-Decreased libido
-CNS effects (HA, sleep disorders, etc.)
-Edema
-Hypotension
19.What are gonadotrophin releasing hormone agonists?: -Synthetic peptide derivative of
gonadotrophin-releasing hormone (GnRH); aka luteinizing hormone-re- leasing hormone (LH-RH)
-Ex/ leuprolide
20.What are the estrogen receptor antagonists/agonists known as selective estrogen receptor
modulators (SERMs)?: -Tamoxifen
-Raloxifene
-Tomremifine
21. What is the MOA of the selective estrogen receptor modulators (SERMs)?-
: -Binds to estrogen receptors (ER) in cytoplasm of breast cancer cells to block estrogen
dependent tumor cell growth in GI and therefore is cytostatic
-These agents maintain bone density (estrogen like effect) and ameliorate factors associated
with coronary heart disease
2/
