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Cancer Chemotherapy Flashcards

1
Q

Describes the proportion of cancer cells that are actively proliferating

A

Tumor growth fraction

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2
Q

Model that describes how tumor growth changes with tumor size
Small tumor has large growth fraction
Growth fraction decreases as tumor gets larger due to limited availability of nutrients and oxygen

A

Gompertzian Growth Model

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3
Q

A model for effect of cytotoxic chemotherapy on tumor size
States that a given dose kills the same fraction regardless of tumor size
E.g. a dose that reduces 10^7 to 10^5 will also reduce that tumor from 10^5 to 10^3

A

Log-kill hypothesis

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4
Q

What is the Gompertzian growth model?

A

States that tumor growth changes with tumor size
E.g. small tumor has large growth fraction

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5
Q

A given dose that reduces 10^7 tumor cells to 10^5, will also reduce that tumor from 10^5 to?

A

10^3 cells

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6
Q

Shared toxicity of cancer mediations that involves an acute inflammation in irradiated tissues when chemotherapy is administered after radiation

A

Radiation recall

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7
Q

Shared toxicity of cancer mediations that involves the cytoplasmic contents of necrotic cells entering circulation and inducing inflammation and toxicity

A

Metabolic abnormalities
(tumor lysis syndrome)

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8
Q

Alkylating agents have this reproductive toxicity

A

Multiple birth defects

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9
Q

Methotrexate has this reproductive toxicity

A

Neural tube defects

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10
Q

Is this a reproductive toxicity of alkylating agents or methotrexate:
Multiple birth defects

A

Alkylating agents

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11
Q

Is this a reproductive toxicity of alkylating agents or methotrexate:
Neural tube defects

A

Methotrexate

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12
Q

What component of nucleosides (sugars and bases) can act as a nucleophile?

A

Both

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13
Q

Both components of nucleosides (sugars and bases) can act as this

A

A nucleophile

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14
Q

Outcome of treatment with alkylating agents that is less repairable/higher cytotoxicity

A

Irreversible crosslinking of two guanines (within and between chains)

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15
Q

A less repairable/higher cytotoxic outcome of alkylating agents is the irreversible crosslinking of ?

A

Two guanines

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16
Q

Cisplatin, Carboplatin, Oxaliplatin, and Cyclophosphamide are this type of antineoplastic agent

A

Alkylating agents

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17
Q

Cisplatin is this type of antineoplastic agent

A

Alkylating agent

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18
Q

Carboplatin is this type of antineoplastic agent

A

Alkylating agent

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19
Q

Oxaliplatin is this type of antineoplastic agent

A

Alkylating agent

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20
Q

Cyclophosphamide is this type of antineoplastic agent

A

Alkylating agent

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21
Q

Busulfan is this type of antineoplastic agent

A

Alkylating agent

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22
Q

Primary toxicity of busulfan (an alkylating agent)

A

Pulmonary fibrosis (“Busulfan lung”)

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23
Q

Carmustine, lomustine, and semustine are this type of neoplastic agent

A

Alkylating agents

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24
Q

Alkylating agent with pulmonary fibrosis as a primary toxicity

A

Busulfan

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25
Q

Primary toxicity of carmustine, lomustine, and semustine (alkylating agents)

A

Bone marrow depression that may be delayed and prolonged

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26
Q

Alkylating agents with bone marrow depression that may be delayed and prolonged as a primary toxicity

A

Carmustine, lomustine, semustine

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27
Q

2 primary toxicities associated with ciplastin, carboplatin, and oxaliplatin (alkylating agents)

A

Nephrotoxicity and Ototoxicity

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28
Q

Alkylating agent that causes powerful nausea and vomiting

A

Cisplatin

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29
Q

Primary toxicity of cisplatin (alkylating agent)

A

Powerful nausea and vomiting
(also nephrotoxicity and ototoxicity)

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30
Q

Nephrotoxicity and ototoxicity are toxicities associated with these alkylating agents

A

Cisplatin, carboplatin, oxaliplatin

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31
Q

Alkylating agents with toxicities involving hemorrhagic cystitis caused by acrolein (a CYP metabolite)

A

Cyclophosphamide, ifosfamide

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32
Q

Primary toxicity associated with cyclophosphamide and ifosfamide (alkylating agents)

A

Hemorrhagic cystitic
caused by acrolein (a CYP metabolite)

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33
Q

Hemorrhagic cystitis may be reduced in patients taking cyclophosphamide or ifosfamide with these

A

Mesna or amifostine (scavenger compound for acrolein)

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34
Q

CYP metabolite that causes hemorrhagic cystitis in patients taking cyclophosphamide or ifosfamide

A

Acrolein

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35
Q

Mesna or amifostine (scavenger compound for acrolein) reduces hemorrhagic cystitis and is required for this alkylating agent

A

Ifosfamide

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36
Q

Dacarbazine and mechlorethamine are alkylating agents with this effect

A

Vesicant (blistering agents)

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37
Q

Alkylating agent that uses phenylalanine transporter to enter cells (should be taken on an empty stomach)

A

Melphalan

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38
Q

Melphalan is an alkylating agent that uses this to enter cells

A

Phenylalanine transporter

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39
Q

Diabetes is a primary toxicity associated with this alkylating agent

A

Streptozocin
action is specific for beta cells of pancreas

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40
Q

Streptozocin is an alkylating agent with this primary toxicity

A

Diabetes
Action is specific for pancreas beta cells

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41
Q

Alkylating agent with risk of opportunistic infections, especially of the lungs

A

Temozolomide

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42
Q

Methotrexate, pemetrexed, and pralatrexate are this type of antimetabolite

A

Antifolates

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43
Q

6-mercaptopurine, Fludarabine, and Cladribine are this type of antimetabolite

A

Purine analogs

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44
Q

5-fluorouracil, capecitabine, cytarabine, azacitidine, and gemcitabine are this type of antimetabolite

A

Pyrimidine analogs

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45
Q

Methotrexate is this type of antineoplastic agent

A

Antifolate

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46
Q

6-Mercaptopurine is this type of antineoplastic agent

A

Purine analog (antimetabolite)

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47
Q

5-fluorouracil is this type of antineoplastic agent

A

Pyrimidine analog (antimetabolite)

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48
Q

Gemcitabine is this type of antineoplastic agent

A

Pyrimidine analog (antimetabolite)

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49
Q

Antifolates are specific for this cell cycle phase

A

S phase

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50
Q

Why are antifolates describes as self-limiting?

A

Inhibition of protein synthesis delays or stalls cancer cell cycle progression by preventing them from entering the vulnerable S phase
Referred to as self-limiting because the agent actually limits its own cell kill rate by delaying cell progression

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51
Q

Antineoplastic agents that are describes as self-limiting

A

Antifolates

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52
Q

Antineoplastic agents that are S-phase specific

A

Antifolates

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53
Q

MOA of methotrexate and pralatrexate

A

Inhibition of dihydrofolate reductase

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54
Q

Methotrexate inhibits this

A

Dihydrofolate reductase

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55
Q

2 drugs that inhibit dihydrofolate reductase

A

Methotrexate and Pralatrexate

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56
Q

MOA of pemetrexed

A

Inhibition of dihydrofolate reductase and thymidylate synthase

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57
Q

Pemetrexed inhibits these 2 enzymes

A

Dihydrofolate reductase
Thymidylate synthase

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58
Q

Antimetabolite that inhibits dihydrofolate reductase and thymidylate synthase

A

Pemetrexed

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59
Q

Main toxicity of antifolates

A

Bone marrow depression

60
Q

Bone marrow depression, neurotoxicity, and nephrotoxicity are toxicities of this type of antineoplastic agent

A

Antifolates

61
Q

Reduced folate that uses the same entry mechanism as methotrexate

A

Leucovorin

62
Q

Leucovorin is used as rescue for this

A

Overcoming methotrexate resistance
Normal cells with normal permeability of methotrexate allow leucovorin to “rescue” normal cells from high dose methotrexate while cancer cells die

63
Q

Cancer cell resistance mechanism of antifolates prevents rescue by this

A

Leucovorin

64
Q

Reduced folate that is used as a “rescue” for normal cells from high dose methotrexate while cancer cells die

A

Leucovorin

65
Q

Leucovorin rescues normal cells from high doses of this antineoplastic agent while cancer cells die

A

Methotrexate (antifolate)

66
Q

Purine analog whose dose should be reduced by 50-70% with concurrent use of allopurinol or febuxostat

A

6-Mercaptopurine

67
Q

6-mercaptopurine is this type of anti-cancer agent

A

Purine analog

68
Q

6-mercaptopurine dose should be reduced by 50-70% with concurrent use of either of these

A

Allopurinol or Febuxostat

69
Q

Allopurinol and febuxostat are inhibitors of xanthine oxidase, which normally inactivates this purine analog

A

6-mercaptopurine

70
Q

Allopurinol and Febuxostat are inhibitors of this enzyme which normally inactivates 6-mercaptopurine

A

Xanthine oxidase

71
Q

Fludarabine is this type of anti-cancer agent

A

Purine analog

72
Q

Toxicity of Fludarabine (purine analog)

A

Neurologic toxicity

73
Q

Purine analog that is not for oral use; gut bacteria convert it to a toxic product

A

Fludarabine

74
Q

Purine analog with neurologic toxicity

A

Fludarabine

75
Q

Cladribine is this type of anti-cancer agent

A

Purine analog

76
Q

Cladribine has this toxicity

A

Immunosuppression
and neurotoxicity

77
Q

Purine analog with immunosuppression as a toxicity

A

Cladribine

78
Q

Pyrimidine analogues inhibit DNA synthesis by blocking this enzyme

A

Thymidylate synthase

79
Q

Pyrimidine analog with these toxicities:
Myelosuppression, coronary vasospasm, ‘foot/hand’ syndrome

A

5-Fluorouracil

80
Q

5-Fluorouracil is this type of anti-cancer agent

A

Pyrimidine analog

81
Q

Pyrimidine analog where hands and feet should be watched carefully

A

5-fluorouracil

82
Q

Pyrimidine analog that is a powerful radiosensitizer (radiation recall)

A

Gemcitabine

83
Q

Antibiotics with the suffix “-rubicin” have this toxicity

A

Intercalate with calcium channels –> Cardiotoxicity

84
Q

Why do antibiotics with the suffix “-rubicin” cause cardiotoxicity?

A

Because they intercalate with calcium channels

85
Q

Antibiotics for cancer that have cumulative lifetime limits

A

Daunorubicin, Doxorubicin, Epirubicin, Idarubicin
“-rubicin”
Due to cardiac toxicity

86
Q

Cancer antibiotic with pulmonary fibrosis and mucocutaneous reactions as toxicities

87
Q

Primary toxicity of Bleomycin

A

Pulmonary fibrosis
“Bleomycin lung”

88
Q

Bleomycin is inactivated by this

A

Hydrolase
Low activity in skin and lungs

89
Q

This should be monitored in patients taking Bleomycin

A

Pulmonary function

90
Q

Cardiac toxicity and radiation recall are toxicities of this cancer antibiotic

A

Daunorubicin

91
Q

Cardiac toxicity with -rubicin use can be reduced by concurrent use of this

A

Iron chelator (dexrazoxane)

92
Q

-rubicin concurrent use of iron chelator (dexrazosane) can reduce this

A

Cardiac toxicity

93
Q

MOA of Vincristine, Vinblastine and Vinorelbine

A

Block formation of mitotic spindles by inhibition of polymerization

94
Q

MOA of Paclitaxel and Docetaxel

A

Promote microtubule polymerization and stabilization, preventing their disassembly leading to accumulation of nonfunctional microtubules (mitosis freezes in metaphase)

95
Q

3 drugs with this MOA:
Block formation of mitotic spindles by inhibition of polymerization

A

Vincristine, Vinblastine, Vinorelbine

96
Q

2 drugs with this MOA:
Promote microtubule polymerization and stabilization, preventing their disassembly leading to accumulation of nonfunctional microtubules (mitosis freezes in metaphase)

A

Paclitaxel, Docetaxel

97
Q

3 microtubule inhibitors that are vesicants

A

Vincristine, Vinblastine, Vinorelbine

98
Q

2 microtubule inhibitors with hypersensitivity reactions

A

Paclitaxel, Docetaxel

99
Q

Microtubule inhibitor with neurotoxicity

A

Vincristine

100
Q

Microtubule inhibitor with myelosuppression

A

Vinblastine
(also vinorelbine)

101
Q

3 toxicities of Paclitaxel and Docetaxel

A

Myelosuppression, Neurotoxicity, Alopecia

102
Q

Primary toxicity of Vincristine

A

Neurotoxicity

103
Q

Primary toxicity of Vinblastine

A

Myelosuppression

104
Q

2 S-phase specific inhibitors of topoisomerase I
Do not relieve torsional strain in DNA, leading to breaks

A

Irinotecan and Topotecan

105
Q

MOA of Irinotecan and Topotecan

A

S-phase specific inhibitors of topoisomerase I

106
Q

Irinotecan and Topotecan are this phase specific inhibitors of topoisomerase I

A

S-phase specific

107
Q

Irinotecan and Topotecan are S-phase specific inhibitors of this

A

Topoisomerase I

108
Q

Topoisomerase inhibitor with life-threatening diarrhea as a toxicity
Responds well to atropine

A

Irinotecan

109
Q

Primary toxicity of topotecan and etoposide

A

Bone marrow depression

110
Q

Anticancer agent that is a S and G2-phase specific inhibitor of topoisomerase II

111
Q

MOA of etoposide

A

S and G2-phase specific inhibitor of topoisomerase II

112
Q

Target of Trastuzumab

A

Human epidermal growth factor receptor 2 (HER2)

113
Q

Human epidermal growth factor receptor 2 (HER2) is a target for this monoclonal antibody

A

Trastuzumab

114
Q

Cancer monoclonal antibody with increased risk of heart failure

A

Trastuzumab

115
Q

Primary toxicity of Trastuzumab

A

Increased risk of heart failure

116
Q

Target for Rituximab

A

CD20 antigen on normal and malignant B cells

117
Q

CD20 antigen on normal and malignant B cells is the target of this monoclonal antibody

118
Q

Bone marrow suppression is the primary toxicity of this monoclonal antibody

119
Q

Primary toxicity of Rituximab

A

Bone marrow suppression

120
Q

Target of Bevacizumab

A

Vascular endothelial growth factor (VEGF); inhibits angiogenesis

121
Q

Vascular endothelial growth factor (VEGF) is the target of this monoclonal antibody

A

Bevacizumab

122
Q

Target of Cetuximab

A

Blocks binding to the epidermal growth factor receptor on cancer cells

123
Q

Monoclonal antibody that blocks binding to the epidermal growth factor receptor on cancer cells

124
Q

Acneiform-type rash is a primary toxicity of this monoclonal antibody

125
Q

Primary toxicity of Cetuximab

A

Aceniform-type rash

126
Q

What is a positive sign of therapy of Cetuximab?

A

Aceniform-type rash

127
Q

Drug names ending in “-nib” are inhibitors of this

A

Targeted kinase inhibitors

128
Q

Drug names ending in “-nib” are toxic to this

A

Heart
(are targeted kinase inhibitors)

129
Q

Targeted kinase inhibitors are often toxic to this

130
Q

Targeted kinase inhibitor:
Rash is common and typically related to stronger therapeutic responses

131
Q

Targeted kinase inhibitor where you should monitor for signs of heart failure and wound-healing complications

132
Q

This is a common side effect of Erlotinib and is typically related to stronger therapeutic responses

133
Q

Primary toxicity of Erlotinib

134
Q

Mechlorethamine + Oncovin/Vincristine + Prednisone + Procarbazine (“MOPP”) is a combination therapy indicated for this

A

Hodgkin’s lymphoma

135
Q

Melanoma changes with this mutation

A

BRAF mutation

136
Q

Cancer that changes with BRAF mutation

137
Q

Breast cancer therapy for ER+/PR+ in premenopause

138
Q

ER antagonist in breast; indicated for breast cancer that expresses ER (ER+)

139
Q

Breast cancer therapy for ER+/PR+ in postmenopause

A

Aromatase inhibitors

140
Q

Block conversion of estrogen precursors (e.g. testosterone) to estradiol and estrone
Reduce concentration of estrogen that promotes growth of breast cancer cells

A

Aromatase inhibitors
Indicated for ER+/PR+ breast cancer postmenopause

141
Q

Breast cancer therapy for ER-/PR-/HER2+

A

Trastuzumab and/or lapatinib, +/- chemotherapy

142
Q

Breast cancer therapy for ER-/PR-/HER2-

A

Chemotherapy
Anthracycline + cyclophosphamide +/- taxane

143
Q

Tamoxifen or Aromatase inhibitors are treatment for this type of breast cancer

144
Q

Trastuzumab and/or lapatinib, +/- chemotherapy, is treatment for this type of breast cancer

A

ER-/PR-/HER2+

145
Q

Chemotherapy (Anthracycline + cyclophosphamide +/- taxane) is treatment for this type of breast cancer

A

ER-/PR-/HER2- (TNBC)

146
Q

Monoclonal antibody that targets HER2, so is used in HER2+ breast cancer, and is contraindicated during pregnancy

A

Trastuzumab

147
Q

Trastuzumab is contraindicated in this

MF2 Pharmacology (14 decks)

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