Anti-Cancer Drugs 1

Question 1

What drugs are the nitrogen mustard alkylating agents?

Answer 1

Cyclophosphamide

ifosfamide

Question 2

What drugs are Nitrosoureas alkylating agents?

Answer 2

Carmustine

lomustine

Question 3

What drugs are classified as alkyl sulfonate alkylating agents?

Answer 3

busulfan

the main use of busulfan is to treat CML

Question 4

What drugs are non-classic alkylating agents?

Answer 4

procarbazine

Question 5

What drugs are platinum analog alkylating agents

Answer 5

cisplatin

Question 6

Methotrexate (MTX) inhibits the formation of?

Answer 6

folate

this is why it is teratogenic

Question 7

F-FU, cytarabine, and gemcitabine are antagonists of what?

Answer 7

Pyrimidine

Question 8

6-MP, 6-TG, and Fludarabine are antagonists of what?

Answer 8

Purine

Question 9

Antimetabolites inhibit what phase of the cell cycle?

Answer 9

S phase (DNA Synthesis)

Question 10

What drugs inhibit S phase?

Answer 10

Topoisomerase I and II inhibitors

Both types of topoisomerase inhibitors cause breaks in the DNA which leads to cell death

Question 11

What drug is specific for the G2 phase of the cell cycle?

Answer 11

Bleomycin

Question 12

What drugs are specific for the M phase of the cell cycle?

what is their target structure?

Answer 12

Vinblastine/vincristine inhibit the formation of microtubules

paclitaxel/docetaxel inhibit the breakdown of microtubules

Question 13

Vincristine

Clinical Use

Side Effects

Answer 13

Vincristine

1. Clinical Use: ALL, rhabodomyosarcoma, Whilm’s tumor (pediatric tumors)
2. Side Effects:
   
   1. Neurological toxicity w/ peripheral sensory neuropathy
   2. paralytic ileus (severe constipation)
   3. SIADH

Question 14

Vinblastine

Clinical Use

Side Effects

Answer 14

Vinblastine

1. Clinical Use:
   
   1. Lymphoma, germ cell, breast ca, Kaposi’s Sarcoma
2. Side Effects:
   
   1. GI disturbances
   2. BM suppression
   3. extravasation leading to cellulitis and phlebitis

Question 15

Paclitaxel

Clinical Use

Side Effects

Answer 15

Paclitaxel

1. Clinical Use
   
   1. ovarian, breast, lung, AIDS related Kaposi’s sarcoma
2. Side Effects
   
   1. BM suppression (neutropenia- treat with filgastrim)
   2. Hypersensitivity rxns (treat with dexamethasone, diphenhydramine, cimetidine)

Question 16

Docetaxel

Clinical Use

Side Effects

Answer 16

Docetaxel

1. Clinical Use: broad coverage
2. Side Effects:
   
   1. BM suppression
   2. Hypersensitivity rxn
   3. neurotoxicity
   4. fluid retention (pre-treat w/ glucocorticoides)
      
      1. pleurall effusion, ascites, peripheral edema, dyspnea at rest, cardiac tamponade

Question 17

Etoposide

MOA

Clinical Use

Side effects

Answer 17

Etoposide

1. MOA: binds and inhibits toposiomerase II causing ds breaks and prevents religation of DNA leading to apoptosis
2. Clinical Use: testicular cancer
3. BM suppression, hypotension, N/V

Question 18

Topotecan

MOA

Clinical Use

Side Effects

Answer 18

Topotecan

1. MOA: binds and inhibits Topoisomerase I (prevents (-) supercoiling
2. Clinica Use: ovarian and SCLC
3. Side effects
   
   1. N/V
   2. Diarrhea treat with loperamide
   3. BM suppression

Question 19

Irinotecan

MOA

Clinical Use

Side Effects

Answer 19

Irinotecan

1. MOA: binds to topoisomerase I
2. Clinical Use: colorectal cancer, gastroesophageal
3. Side Effects:
   
   1. N/V
   2. Diarrhea
   3. BM supression

Question 20

Daunorubicin/Doxorubinicin

Clinical Use

Side Effects

Answer 20

Daunorubicin/Doxorubinicin

1. mainly used in AML, ALL
2. Cardiotoxicity
   
   1. Damage is caused by free radicals
      
      1. acute (2-3 adys)
      2. chronic (DCM)
   2. prevent with Dexrazoxane

Question 21

Dactinomycin (actinomycin D)

MOA

Clinical Use

Side Effects

Answer 21

Dactinomycin (actinomycin D)

1. MOA: binds to DNA through intercalation which prevents DNA synthesis
2. Clinical Use:
   
   1. Childhood cancerrs (Whilm’s tumor, rhabdomyosarcoma), Ewing’s Sarcoma
3. SE: N/V, BM suppression

Question 23

Bleomycin

MOA

Clinical Use

Side Effects

Answer 23

Bleomycin

1. MOA: binds to DNA anc creates a DNA-Bleomycin-Fe(II) complex that oxidizes andd creates free radicals (Superoxide and hydroxide) which breaks DNA
2. Clinical Use: lymphomas, germ cell (testis, ovary)
3. Side Effects:
   
   1. Pulmonary Toxicity
      
      1. can lead to pulmonary fibrosis
   2. Cutaneous (skin) toxicity
      
      1. hyperpigmentation, skin ulcerations, flagellate dermatitis
   3. hypersensitivity

Question 24

Mitomycin

MOA

Clinical Use

Side Effects

Answer 24

Mitomycin:

1. MOA: enzymatic metabolic activation that generates an alkylating agent that cross-links DNA
2. CU: various
3. Hemolytic-uremic syndrome
   
   1. anemia, thrombocytopenia, renal failure due to damage of endothelial cells by drug toxicity

Question 25

Tamoxifen MOA Clinical Use Side Effects

Answer 25

Tamoxifen 1. MOA: Estrogen antagonist (SERM) in the breast tissue 1. competitively binds to estrogen receptor 2. CU: breast cancer that is HR (+), ER (+) 3. SE: hot flashes, vaginal discharge/bleeding, thromboembolism, increased risk of uterine cancers

Question 26

Raloxifene Clinical Use

Answer 26

Raloxifene used for treating osteoperosis and reducing the risk of breast cancer in postmenopausal women

Question 27

Anastrozole, letrozole, exemestane MOA Clinical Use Side effects

Answer 27

1. selectively and competitively binds to and inactivates aromatase 1. androgens can not be converted into estrogen 2. CU: HR (+) breast cancer in postmenopausal women 3. decreased bone minearal density, hypercholestrolemia, and ischemic cardiovascular disease and angina