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Antineoplastics Flashcards

1
Q

Mechlorethamine: (explain/give the following) a. Class b. Mechanism c. Pharmacokinetics d. Therapeutic use e. adverse effects

A

a. Alkylating agent (nitrogen mustard) b. Type I. Bifunctional alkylating agent: produces cross-links in DNA. c. IV. No CNS penetration. Highly reactive. Disappears from blood in seconds to minutes d. Hodgkin’s and non-hodgkin’s lymphoma e. nausea/vomiting, myelosuppression, mild alopecia

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2
Q

Name three alkylating agent antineoplastic drugs

A
  1. mechlorethamine (nitrogen mustard) 2. cyclophosphamide (nitrogen mustard) 3. carmustine (BCNU) (nitrosourea)
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3
Q

Name two vinca alkaloid antineoplastic drugs

A
  1. Vinblastine 2. Vincristine
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4
Q

Name five antimetabolite antineoplastic drugs

A
  1. methotrexate (MTX) 2. 5-fluorouracil (5-FU) 3. cytarabine (Ara-C) 4. mercaptopurine (MCP) 5. hydroxyurea
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5
Q

Name one taxane antineoplastic drug

A
  1. Paclitaxel
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6
Q

Name four antiestrogenic antineoplastic drugs and the sub-class of each

A
  1. temoxifen (TAM) - nonsteroidal antiestrogen 2. letrozole - aromatase (CYP19) inhibitor 3. leuprolide - GnRH analog 4. flutamide - nonsteroidal antiandrogen
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7
Q

Name one corticosteroid antineoplastic drug

A
  1. prednisone
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8
Q

Name one atypical alkylating agent antineoplastic drug

A
  1. procarbazine
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9
Q

Name one metal complex used as an antineoplastic drug

A
  1. cisplatin (platinum coordination complex)
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10
Q

Name one monoclonal antibody used as an antineoplastic drug

A
  1. trastuzumab (Herceptin)
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11
Q

Name two antibiotic agents used as antineoplastic drugs

A
  1. doxorubicin 2. bleomycin (BLM)
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12
Q

Name one epipodphyllotoxin used as an antineoplastic drug

A
  1. etoposide (VP16)
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13
Q

Name one BRM used as an antineoplastic drug

A
  1. filgrastim
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14
Q
A
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15
Q

Mechlorethamine: mechanism of action

A

Type I (nitrogen mustard). Bifunctional alkylating agent: produces cross-links.

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16
Q

Cyclophosphamide: mechanism of action

A

Type III (nitrogen mustard). Prodrug activated in liver by CYP450 → active compound phosphoramide mustard acts as akylating agent. Acrolein (byproduct) causes bladder toxicity

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17
Q

Mechanism of action: carmustine (BCNU)

A

alkylating agent. produces cross-links in DNA

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18
Q

Mechanism of action: Methotrexate

A

antimetabolite:

Binds to DHFR → blocks formation to FH4 → blocks purine and pyrimidine synthesis

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19
Q

Mechanism of action: 5-fluorouracil (5-FU)

A

antimetabolite

Pyrimidine analog → activated to FUTP → inhibits RNA synthesis
Pyrimidine analog → activated to FdUMP → interferes with thymidylate synthase → inhibit DNA synthesis

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20
Q

Mechanism of action: cytarabine (Ara-C)

A

antimetabolite

Pyrimidine (cytadine) analog → competes for phosphorylation of cytidine → also competes with cytidine for incorporation into DNA → causes chain termination

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21
Q

Mechanism of action: mercaptopurine

A

antimetabolite
Purine analog → converted in cells (by HGPRT) to ribonucleotide that inhibits purine synthesis. Further converted and misincorporated into DNA and RNA

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22
Q

Mechanism of action: hydroxyurea

A

antimetabolite

Substituted urea → inhibits ribonucleotide reductase → blocks conversion to dNTPs → prevents DNA synthesis → arrests cell at G1-S interface

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23
Q

Mechanism of action: vinblastine

A

vinca alkaloid

Binds tubulin → prevents formation of microtubules and mitotic spindle

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24
Q

Mechanism of action: vincristine

A

vinca alkaloid

Binds tubulin → prevents formation of microtubules and mitotic spindle

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25
Q

Mechanism of action: paclitaxel

A

taxane

Binds tubulin beta-subunity → enhances assembly and stability of microtubules → arrests cells in late G2 phase (G2/M interface)

Can also interfere with DNA repair – intensifying effect of cisplatin or cyclophosphamide

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26
Q

Mechanism of action: doxorubicin

A

Antibiotic

Antitumor antibiotic (similar to tetracyclines) → intercalates in DNA (distorts helix). Also causes lipid peroxidation and ROS generation. Also binds DNA topoisomerase II → prevents resealing of DNA strand breaks

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27
Q

Mechanism of action: bleomycin (BLM)

A

Antibiotic

Iron-containing glycopeptide that binds to DNA → causes oxidative-like damage to DNA → DNA strand breaks (single and double)

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28
Q

Mechanism of action: etoposide (VP16)

A

Epipodphyllotoxin

Irreversible stabilizes DNA-topoisomerase II complexes → results in dsDNA breaks that cannot be repeaired → arrests cell in late G2 phase (G2/M interface)

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29
Q

Mechanism of action: fligrastim (G-CSF)

A

BLM

Granulocyte colony stimulating factor → promotes neutrophil progenitors → expands absolute population of neutrophils → counteracts the effects of chemotherapy-induced neutropenia

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30
Q

Mechanism of action: trastuzumab (Herceptin)

A

Monoclonal antibody

Monoclonal antibody → binds HER2 receptor (human epidermal growth factor receptor 2) → blocks proliferation of cells (25-30% of metastatic breast cancers express HER2R

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31
Q
A
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32
Q

Mechanism of action: cisplatin

A

Metal complex

Platinum coordination complex → hydrolysis yields activated species which cross-links DNA → inhibits transcription, repair, protein recognition → produces apoptosis

Also covalently binds thioredoxin reductase (TrxR – overexpressed by many cancers) → directly promotes apoptosis

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33
Q

Mechanism of action: procarbazine

A

atypical alkylating agent

activated in vivo by liver to methylating agent → chromosomal damage

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34
Q

Mechanism of action: prednisone

A

Corticosteroid

Bind steroid receptors → modulate cell growth, including: arrest cells at G1, depress growth gene expression, induce nucleases (promote cell lysis)

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35
Q

Mechanism of action: tamoxifen (TAM)

A

Antiestrogenic - non-steroidal

Nonsteroidal antiestrogen → competitively blocks estrogen receptors in breast tissue. → cells halt at G0/G1 interface. Also elevates sex hormone-binding globulin → decreases free estradiol levels

Off-label use: estrogen agonist in bone tissue → may prevent post-menopausal osteoporosis

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36
Q

Mechanism of action: letrozole

A

Antiestrogenic

Aromatase (CYP19) inhibitor → binds heme domain → blocks conversion of androgens to estrogens → prevents stimulation of ER+ cells

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37
Q

Mechanism of action: leuprolide

A

Antiandrogenic

GnRH analog → initially stimulates LH and FSH → testosterone surge (and disease flare) → LH/FSH burnout after 2-4 wks → decrease testosterone to castration levels

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38
Q

Mechanism of action: flutamide

A

Antiandrogenic

Nonsteroidal antiandrogen → blocks androgen receptors

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39
Q

Therapeutic use: mechlorethamine

A

Hodgkin’s and non-Hodgkin’s lymphoma

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40
Q

Therapeutic use: cyclophosphamide

A

Broad spectrum anti-cancer (most widely used alkylating agent)

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41
Q

Therapeutic use: carmustine (BCNU)

A

Brain tumors

multiple myeloma

melanoma

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42
Q

Therapeutic use: methotrexate

A

Acute lymphblastic leukemia (ALL)
Choriocarcinoma

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43
Q

Therapeutic use: 5-fluorouracil (5-FU)

A

Broad spectrum: stomach, colon, pancreas, overy, head, neck, breast, bladder. Basal cell carcinoma.
**GI and breast are most common applications**

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44
Q

Therapeutic use: cytarabine (Ara-C)

A

Acute leukemias
Acute myelocytic leukemia (AML)
Lymphomas
Head and neck cancer

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45
Q

Therapeutic use: mercaptopurine

A

Acute leukemias

Chronic granulocytic anemia

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46
Q

Therapeutic use: hydroxyurea

A

Granulocytic leukemia

47
Q

Therapeutic use: vinblastine

A

Lymphomas
Breast cancer
Testicular cancer
Bladder cancer

48
Q

Therapeutic use: vincristine

A

Acute lymphocytic leukemia
Lymphomas
Wilm’s tumor
Neuroblastoma

49
Q

Therapeutic use: paclitaxel

A

Ovarian cancer (with cisplatin) → high TGF-beta tumors

50
Q

Therapeutic use: doxorubicin

A 
Wide spectrum (most prescribed in its class)
Lymphomas, breast, ovary, small cell lung
51
Q

Therapeutic use: bleomycin

A

Germ cell tumors of testes and ovaries
Head, neck, lung, lymphomas
Skin, esophagus, genitourinary

52
Q

Therapeutic use: etoposide (VP16)

A

Lymphomas, acute leukemia, small cell lung, testis, Kaposi’s sarcoma

53
Q

Therapeutic use: filgrastim (G-CSF)

A

Lessens risk of infection and restores neutrophil count enough for patients to resume therapies that otherwise suppress bone marrow

54
Q

Therapeutic use: trastuzumab (Herceptin)

A

Metastatic breast cancer (1st line with paclitaxel)
Other HER2-positive cancers

55
Q

Therapeutic use: cisplatin

A

Wide anti-tumor spectrum
Testicular cancer (with etoposide and belomycin)
Ovarian cancer (cisplatin + paclitaxel)
Head, neck, bladder, small cell lung, colon, esophagus

56
Q

Therapeutic use: procarbazine

A

Hodgkin’s lymphoma

57
Q

Therapeutic use: prednisone

A

Lymphoma, lymphocytic leukemia
Breast cancer

Palliative effects: anti-emetic, stimulates appetite, anti-inflammatory

58
Q

Therapeutic use: tamoxifen (TAM)

A

Advanced post-menopausal breast cancer (adjuvant, in combo with surg/rad/chemo)
Pre-menopausal metastatic breast cancer
Breast cancer prophylaxis for high-risk populations

59
Q

Therapeutic use: letrozole

A

Post-menopausal locally-advanced or metastatic breast cancer (1st line treatment)

60
Q

Therapeutic use: leuprolide

A

Prostate cancer (advanced, hormonally-responsive – 1st line)

61
Q

Therapeutic use: flutamide

A

Metastatic prostate cancer (used in combination with GnRH agonist or a 2nd line therapy)

62
Q

Which of the alkylating agents has the greatest CNS penetration?

A

carmustine (BCNU)

63
Q

Adverse effects: alkylating agents

A
  1. Nausea/vomiting
  2. myelosuppression
  3. alopecia

mechlorethamine: 1, 2, mild 3
cyclophosphamide: 1, limited 2, 3. Also bladder toxicity
carmustine: 1, delayed 2

64
Q

Which of the alkylating agents has bladder toxicity as a major adverse effect? What is used to counter it?

A

Cyclophosphamide

counteract with: mesna

65
Q

What is leucovorin?

A

Example of rescue

leucovorin = folinic acid, does not require DHFR

Used following high-dose methotrexate therapy

Normal cells have greater capacity to take up leucovorin than tumor cells

66
Q

Side effects: methotrexate

A

Intestinal epithelial damage (diarrhea, bleeding), bone marrow supporession, renal tubular necrosis (counter: alkalinize urine), displacement of other drugs

67
Q

All antimetabolites are specific for what phase of the cell cycle?

68
Q

Adverse effects: 5-fluorouracil

A

(usually delayed): Nausea, anorexia, diarrhea, myelosuppression

69
Q

Adverse effects: cytarabine (Ara-C)

A

myelosuppression (dose-limiting)
Neurotoxicity

70
Q

Adverse effects: mercaptopurine

A

Bone marrow suppression, vomiting, nausea, anorexia, jaundice

TPMT polymorphism related toxicity

71
Q

Adverse effects: hydroxyurea

A

Hematopoietic depression, GI disturbances

72
Q

Adverse effects: vinblastine

A

Strong myelosuppression
Epithelial ulcerations

73
Q

Adverse effects: vincristine

A

Less myelosuppression than vinblastine
Alopecia
Neuromuscular abnormalities and peripheral neuropathy
Bronchospasm, cramps, nausea/vomiting/diarrhea

74
Q

Adverse effects: paclitaxel

A

Leukopenia (dose-limiting)
Peripheral neuropathy
Myalgia, arthralgia
Hypersensitivity, alopecia, nausea/vomiting, mild cardiotoxicity

75
Q

Adverse effects: doxorubicin

A

Dilated cardiomyopathy (cumulative) → due to ROS and low GSH peroxidase in heart tissue → reduce effect with detrazoxane (Fe chelating agent)
Bone marrow depression
Alopecia
GI problems

76
Q

Adverse effects: bleomycin (BLM)

A

Minimal myelosuppression
***Pulmonary toxicity (cumulative, fatal) → due to low levels of bleomycin hydrolase
Skin vesiculation, hyperpigmentation
Fever, alopecia

77
Q

Which antineoplastic has the unique adverse effect of pulmonary toxicity

A

bleomycin (BLM)

78
Q

Adverse effects: etoposide (VP16)

A

leukopenia (dose-limiting), nausea/vomiting/diarrhea, alopecia

79
Q

Adverse effects: filgrastim (G-CSF)

A 
Bone pain (33%)
Hyperuricemia, leukocytosis
80
Q

Adverse effects: trastuzumab (Herceptin)

A

Cardiomyopathy (reversible)
Hypersensitivity (severe)
Infusion reactions (fever, chills)

81
Q

Adverse effects: cisplatin

A

**Nephrotoxicity (dose-related, lethal)
Ototoxicity (tinnitus, HF loss)
Peripheral neuropathy
Electrolyte disturbances
Nause/vomiting (100%)
Myelosuppression (mild/moderate)

82
Q

Which antineoplastic drug has the dose-related nephrotoxicity as a major adverse effect?

83
Q

Adverse effects: procarbazine

A

Myelosuppression, nausea/vomiting
Secondary malignancies (prolonged use)
Central & peripheral neurotoxicity

84
Q

Adverse effects: prednisone

A

Immunosuppression
Myelosuppression (limited)
Weight gain, fluid retention, psychological effects

85
Q

Adverse effects: tamoxifen (TAM)

A

nausea/vomiting, menopause-like symptoms (hot flashes), fatigue, bone/musculoskeletal pain
May increase risk of uterine/endometrial cancer (prolonged use → increases cell growth in these tissues)

86
Q

Adverse effects: letrozole

A

Hot flashes
Nausea
Fatigue
Bone/musculoskeletal pain
Decreased bone mineral density

87
Q

Adverse effects: leuprolide

A

Disease flare (1st 1-2 wks)
Hot flashes
Impotence

88
Q

Adverse effects: flutamide

A

Gynecomastia, impotence
Diarrhea
Hepatotoxicity (rare)

89
Q

What is the active form of tamoxifen (TAM)?

A

endoxifen, converted from tamoxifen by CYP2D6

2D6 ultrafast metabolizers experience greater adverse effects

90
Q

Which antineoplastic drugs destabilize microtubles?

A

Vinca alkaloids:

vinblastine

vincristine

91
Q

Which antineoplastic drugs stabilize microtubules?

A

Taxanes:

paclitaxel

locks cells in the G2/M interface -> may have some use as a radiosensitizer since cells may be more vulnerable to radiation therapy here

92
Q

Which anti-neoplastic drug has anti-angiogenic properties?

A

doxorubicin

93
Q

Which drug has major dilated cardiomyopathy as a side effect and state the reason for this specific side effect

A

Doxorubicin - generates H2O2, which is normally quenched by glutathione peroxidase. Cardiac muscle expresses little of this enzyme and is therefore especially vulnerable.

dexrazoxane can be used to lessen cardiomyopathy (chelates Fe -> preventing free radical damage)

94
Q

Which antineoplast requires chelated Fe?

A

Bleomycin (BLM)

95
Q

What is a BRM?

A

Biological response modifier - naturally occurring proteins or therapeutic molecules designed to mimic or impact natural proteins

example: filgrastim (G-CSF)

96
Q

Which enzyme is responsible for the conversion of androgens to estrogens?

A

aromatase (CYP19)

97
Q

Multi-drug resistance (MDR) to antineoplastic drugs is accomplished primarily by what mechanism? For which classes of drugs is this a prominent problem?

A

ATP-dependent drug efflux pumps

example: p-glycoprotein

Especially prominent for: vinca alkaloids, antibiotics, etoposide, taxanes

98
Q

What is sequential blockade?

A

Simultaneous action of two inhibitors acting on different steps of a linear metabolic pathway

examples: hydroxyurea + cytarabine

methotrexate + 5-FU

99
Q

What is concurrent inhibition?

A

Inhibitors block two separate pathways that lead to the same end product

examples: none

100
Q

What is complementary inhibition?

A

One drug affects the function of an end-product, and the other drug affects the synthesis of that end product

example: cytarabine + doxorubicin

cytarabine inhibits DNA synthesis, doxorubicin cause DNA damage

101
Q

What is rescue?

A

Counteract a major toxicity or particular effect on normal cells so that dose or length of treatment may be increased (or continue)

examples: methotrexate + leucovorin

bone marrow transplant

102
Q

What is synchronization?

A

Synchronize cells so that most are in the same phase. Then use a drug specific to that phase to kill as many tumor cells as possible.

example: low-dose 5-FU to block in S-phase, followed by high-dose cytarabine to kill cells in S-phase

103
Q

What is recruitment?

A

Mobilize slowly-proliferating or G0 cells back into the cell cycle so that they are more vulnerable to therapy

example: cycle-nonspecific (alkylating agent), following by cycle-specific drug

104
Q

Which antineoplastic drugs are known to have a high risk of secondary malignancy in humans (3)

A

mechlorethamine

carmustine

etoposide

105
Q

Killing of tumors follows what order of kinetics?

A

First-order kinetics

(constant dose of drug kills a constant fraction of tumor cells)

106
Q

Define Class I antineoplastic drug

A

Cell cycle-nonspecific

107
Q

Define Class II antineoplastic drug

A

Cell cycle-specific, phase-specific

108
Q

Define class III antineoplastic drug

A

Cycle-specific, phase-nonspecific

109
Q

Which Class II drugs act in:

  1. G1 phase
  2. S phase
  3. G2 phase
  4. M phase
A
  1. prednisone
  2. cytarabine, fluorouracil, methotrexate, mercaptopurine, hydroxyurea
  3. bleomycin, etoposide, paclitaxel
  4. vinblastine, vincristine
110
Q

Class II drugs are usually administered how often?

A

Continuous infusion or frequent small dose

111
Q

Class III drugs are usually administered how often?

A

single large dose - to take advantage of their sparing effect of normal cells that may be in G0 during treatment

113
Q

Define IC90

A

The dose of an antineoplastic drug that results in 90% reduction in a cell population (1 log kill)

114
Q

2-log kill results in the death of what percentage of a cell population?

FPP_MSS (30 decks)

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