Cancer Chemotherapy Flashcards
1
Q
Describes the proportion of cancer cells that are actively proliferating
A
Tumor growth fraction
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
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
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
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
6
Q
Shared toxicity of cancer mediations that involves an acute inflammation in irradiated tissues when chemotherapy is administered after radiation
A
Radiation recall
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)
8
Q
Alkylating agents have this reproductive toxicity
A
Multiple birth defects
9
Q
Methotrexate has this reproductive toxicity
A
Neural tube defects
10
Q
Is this a reproductive toxicity of alkylating agents or methotrexate:
Multiple birth defects
A
Alkylating agents
11
Q
Is this a reproductive toxicity of alkylating agents or methotrexate:
Neural tube defects
A
Methotrexate
12
Q
What component of nucleosides (sugars and bases) can act as a nucleophile?
A
Both
13
Q
Both components of nucleosides (sugars and bases) can act as this
A
A nucleophile
14
Q
Outcome of treatment with alkylating agents that is less repairable/higher cytotoxicity
A
Irreversible crosslinking of two guanines (within and between chains)
15
Q
A less repairable/higher cytotoxic outcome of alkylating agents is the irreversible crosslinking of ?
A
Two guanines
16
Q
Cisplatin, Carboplatin, Oxaliplatin, and Cyclophosphamide are this type of antineoplastic agent
A
Alkylating agents
17
Q
Cisplatin is this type of antineoplastic agent
A
Alkylating agent
18
Q
Carboplatin is this type of antineoplastic agent
A
Alkylating agent
19
Q
Oxaliplatin is this type of antineoplastic agent
A
Alkylating agent
20
Q
Cyclophosphamide is this type of antineoplastic agent
A
Alkylating agent
21
Q
Busulfan is this type of antineoplastic agent
A
Alkylating agent
22
Q
Primary toxicity of busulfan (an alkylating agent)
A
Pulmonary fibrosis (“Busulfan lung”)
23
Q
Carmustine, lomustine, and semustine are this type of neoplastic agent
A
Alkylating agents
24
Q
Alkylating agent with pulmonary fibrosis as a primary toxicity
A
Busulfan
25
Primary toxicity of carmustine, lomustine, and semustine (alkylating agents)
Bone marrow depression that may be delayed and prolonged
26
Alkylating agents with bone marrow depression that may be delayed and prolonged as a primary toxicity
Carmustine, lomustine, semustine
27
2 primary toxicities associated with ciplastin, carboplatin, and oxaliplatin (alkylating agents)
Nephrotoxicity and Ototoxicity
28
Alkylating agent that causes powerful nausea and vomiting
Cisplatin
29
Primary toxicity of cisplatin (alkylating agent)
Powerful nausea and vomiting
(also nephrotoxicity and ototoxicity)
30
Nephrotoxicity and ototoxicity are toxicities associated with these alkylating agents
Cisplatin, carboplatin, oxaliplatin
31
Alkylating agents with toxicities involving hemorrhagic cystitis caused by acrolein (a CYP metabolite)
Cyclophosphamide, ifosfamide
32
Primary toxicity associated with cyclophosphamide and ifosfamide (alkylating agents)
Hemorrhagic cystitic
caused by acrolein (a CYP metabolite)
33
Hemorrhagic cystitis may be reduced in patients taking cyclophosphamide or ifosfamide with these
Mesna or amifostine (scavenger compound for acrolein)
34
CYP metabolite that causes hemorrhagic cystitis in patients taking cyclophosphamide or ifosfamide
Acrolein
35
Mesna or amifostine (scavenger compound for acrolein) reduces hemorrhagic cystitis and is required for this alkylating agent
Ifosfamide
36
Dacarbazine and mechlorethamine are alkylating agents with this effect
Vesicant (blistering agents)
37
Alkylating agent that uses phenylalanine transporter to enter cells (should be taken on an empty stomach)
Melphalan
38
Melphalan is an alkylating agent that uses this to enter cells
Phenylalanine transporter
39
Diabetes is a primary toxicity associated with this alkylating agent
Streptozocin
action is specific for beta cells of pancreas
40
Streptozocin is an alkylating agent with this primary toxicity
Diabetes
Action is specific for pancreas beta cells
41
Alkylating agent with risk of opportunistic infections, especially of the lungs
Temozolomide
42
Methotrexate, pemetrexed, and pralatrexate are this type of antimetabolite
Antifolates
43
6-mercaptopurine, Fludarabine, and Cladribine are this type of antimetabolite
Purine analogs
44
5-fluorouracil, capecitabine, cytarabine, azacitidine, and gemcitabine are this type of antimetabolite
Pyrimidine analogs
45
Methotrexate is this type of antineoplastic agent
Antifolate
46
6-Mercaptopurine is this type of antineoplastic agent
Purine analog (antimetabolite)
47
5-fluorouracil is this type of antineoplastic agent
Pyrimidine analog (antimetabolite)
48
Gemcitabine is this type of antineoplastic agent
Pyrimidine analog (antimetabolite)
49
Antifolates are specific for this cell cycle phase
S phase
50
Why are antifolates describes as self-limiting?
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
51
Antineoplastic agents that are describes as self-limiting
Antifolates
52
Antineoplastic agents that are S-phase specific
Antifolates
53
MOA of methotrexate and pralatrexate
Inhibition of dihydrofolate reductase
54
Methotrexate inhibits this
Dihydrofolate reductase
55
2 drugs that inhibit dihydrofolate reductase
Methotrexate and Pralatrexate
56
MOA of pemetrexed
Inhibition of dihydrofolate reductase and thymidylate synthase
57
Pemetrexed inhibits these 2 enzymes
Dihydrofolate reductase
Thymidylate synthase
58
Antimetabolite that inhibits dihydrofolate reductase and thymidylate synthase
Pemetrexed
59
Main toxicity of antifolates
Bone marrow depression
60
Bone marrow depression, neurotoxicity, and nephrotoxicity are toxicities of this type of antineoplastic agent
Antifolates
61
Reduced folate that uses the same entry mechanism as methotrexate
Leucovorin
62
Leucovorin is used as rescue for this
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
Cancer cell resistance mechanism of antifolates prevents rescue by this
Leucovorin
64
Reduced folate that is used as a "rescue" for normal cells from high dose methotrexate while cancer cells die
Leucovorin
65
Leucovorin rescues normal cells from high doses of this antineoplastic agent while cancer cells die
Methotrexate (antifolate)
66
Purine analog whose dose should be reduced by 50-70% with concurrent use of allopurinol or febuxostat
6-Mercaptopurine
67
6-mercaptopurine is this type of anti-cancer agent
Purine analog
68
6-mercaptopurine dose should be reduced by 50-70% with concurrent use of either of these
Allopurinol or Febuxostat
69
Allopurinol and febuxostat are inhibitors of xanthine oxidase, which normally inactivates this purine analog
6-mercaptopurine
70
Allopurinol and Febuxostat are inhibitors of this enzyme which normally inactivates 6-mercaptopurine
Xanthine oxidase
71
Fludarabine is this type of anti-cancer agent
Purine analog
72
Toxicity of Fludarabine (purine analog)
Neurologic toxicity
73
Purine analog that is not for oral use; gut bacteria convert it to a toxic product
Fludarabine
74
Purine analog with neurologic toxicity
Fludarabine
75
Cladribine is this type of anti-cancer agent
Purine analog
76
Cladribine has this toxicity
Immunosuppression
and neurotoxicity
77
Purine analog with immunosuppression as a toxicity
Cladribine
78
Pyrimidine analogues inhibit DNA synthesis by blocking this enzyme
Thymidylate synthase
79
Pyrimidine analog with these toxicities:
Myelosuppression, coronary vasospasm, 'foot/hand' syndrome
5-Fluorouracil
80
5-Fluorouracil is this type of anti-cancer agent
Pyrimidine analog
81
Pyrimidine analog where hands and feet should be watched carefully
5-fluorouracil
82
Pyrimidine analog that is a powerful radiosensitizer (radiation recall)
Gemcitabine
83
Antibiotics with the suffix "-rubicin" have this toxicity
Intercalate with calcium channels --> Cardiotoxicity
84
Why do antibiotics with the suffix "-rubicin" cause cardiotoxicity?
Because they intercalate with calcium channels
85
Antibiotics for cancer that have cumulative lifetime limits
Daunorubicin, Doxorubicin, Epirubicin, Idarubicin
"-rubicin"
Due to cardiac toxicity
86
Cancer antibiotic with pulmonary fibrosis and mucocutaneous reactions as toxicities
Bleomycin
87
Primary toxicity of Bleomycin
Pulmonary fibrosis
"Bleomycin lung"
88
Bleomycin is inactivated by this
Hydrolase
Low activity in skin and lungs
89
This should be monitored in patients taking Bleomycin
Pulmonary function
90
Cardiac toxicity and radiation recall are toxicities of this cancer antibiotic
Daunorubicin
91
Cardiac toxicity with -rubicin use can be reduced by concurrent use of this
Iron chelator (dexrazoxane)
92
-rubicin concurrent use of iron chelator (dexrazosane) can reduce this
Cardiac toxicity
93
MOA of Vincristine, Vinblastine and Vinorelbine
Block formation of mitotic spindles by inhibition of polymerization
94
MOA of Paclitaxel and Docetaxel
Promote microtubule polymerization and stabilization, preventing their disassembly leading to accumulation of nonfunctional microtubules (mitosis freezes in metaphase)
95
3 drugs with this MOA:
Block formation of mitotic spindles by inhibition of polymerization
Vincristine, Vinblastine, Vinorelbine
96
2 drugs with this MOA:
Promote microtubule polymerization and stabilization, preventing their disassembly leading to accumulation of nonfunctional microtubules (mitosis freezes in metaphase)
Paclitaxel, Docetaxel
97
3 microtubule inhibitors that are vesicants
Vincristine, Vinblastine, Vinorelbine
98
2 microtubule inhibitors with hypersensitivity reactions
Paclitaxel, Docetaxel
99
Microtubule inhibitor with neurotoxicity
Vincristine
100
Microtubule inhibitor with myelosuppression
Vinblastine
(also vinorelbine)
101
3 toxicities of Paclitaxel and Docetaxel
Myelosuppression, Neurotoxicity, Alopecia
102
Primary toxicity of Vincristine
Neurotoxicity
103
Primary toxicity of Vinblastine
Myelosuppression
104
2 S-phase specific inhibitors of topoisomerase I
Do not relieve torsional strain in DNA, leading to breaks
Irinotecan and Topotecan
105
MOA of Irinotecan and Topotecan
S-phase specific inhibitors of topoisomerase I
106
Irinotecan and Topotecan are this phase specific inhibitors of topoisomerase I
S-phase specific
107
Irinotecan and Topotecan are S-phase specific inhibitors of this
Topoisomerase I
108
Topoisomerase inhibitor with life-threatening diarrhea as a toxicity
Responds well to atropine
Irinotecan
109
Primary toxicity of topotecan and etoposide
Bone marrow depression
110
Anticancer agent that is a S and G2-phase specific inhibitor of topoisomerase II
Etoposide
111
MOA of etoposide
S and G2-phase specific inhibitor of topoisomerase II
112
Target of Trastuzumab
Human epidermal growth factor receptor 2 (HER2)
113
Human epidermal growth factor receptor 2 (HER2) is a target for this monoclonal antibody
Trastuzumab
114
Cancer monoclonal antibody with increased risk of heart failure
Trastuzumab
115
Primary toxicity of Trastuzumab
Increased risk of heart failure
116
Target for Rituximab
CD20 antigen on normal and malignant B cells
117
CD20 antigen on normal and malignant B cells is the target of this monoclonal antibody
Rituximab
118
Bone marrow suppression is the primary toxicity of this monoclonal antibody
Rituximab
119
Primary toxicity of Rituximab
Bone marrow suppression
120
Target of Bevacizumab
Vascular endothelial growth factor (VEGF); inhibits angiogenesis
121
Vascular endothelial growth factor (VEGF) is the target of this monoclonal antibody
Bevacizumab
122
Target of Cetuximab
Blocks binding to the epidermal growth factor receptor on cancer cells
123
Monoclonal antibody that blocks binding to the epidermal growth factor receptor on cancer cells
Cetuximab
124
Acneiform-type rash is a primary toxicity of this monoclonal antibody
Cetuximab
125
Primary toxicity of Cetuximab
Aceniform-type rash
126
What is a positive sign of therapy of Cetuximab?
Aceniform-type rash
127
Drug names ending in "-nib" are inhibitors of this
Targeted kinase inhibitors
128
Drug names ending in "-nib" are toxic to this
Heart
(are targeted kinase inhibitors)
129
Targeted kinase inhibitors are often toxic to this
Heart
130
Targeted kinase inhibitor:
Rash is common and typically related to stronger therapeutic responses
Erlotinib
131
Targeted kinase inhibitor where you should monitor for signs of heart failure and wound-healing complications
Sorafenib
132
This is a common side effect of Erlotinib and is typically related to stronger therapeutic responses
Rash
133
Primary toxicity of Erlotinib
Rash
134
Mechlorethamine + Oncovin/Vincristine + Prednisone + Procarbazine ("MOPP") is a combination therapy indicated for this
Hodgkin's lymphoma
135
Melanoma changes with this mutation
BRAF mutation
136
Cancer that changes with BRAF mutation
Melanoma
137
Breast cancer therapy for ER+/PR+ in premenopause
Tamoxifen
138
ER antagonist in breast; indicated for breast cancer that expresses ER (ER+)
Tamoxifen
139
Breast cancer therapy for ER+/PR+ in postmenopause
Aromatase inhibitors
140
Block conversion of estrogen precursors (e.g. testosterone) to estradiol and estrone
Reduce concentration of estrogen that promotes growth of breast cancer cells
Aromatase inhibitors
Indicated for ER+/PR+ breast cancer postmenopause
141
Breast cancer therapy for ER-/PR-/HER2+
Trastuzumab and/or lapatinib, +/- chemotherapy
142
Breast cancer therapy for ER-/PR-/HER2-
Chemotherapy
Anthracycline + cyclophosphamide +/- taxane
143
Tamoxifen or Aromatase inhibitors are treatment for this type of breast cancer
ER+/PR+
144
Trastuzumab and/or lapatinib, +/- chemotherapy, is treatment for this type of breast cancer
ER-/PR-/HER2+
145
Chemotherapy (Anthracycline + cyclophosphamide +/- taxane) is treatment for this type of breast cancer
ER-/PR-/HER2- (TNBC)
146
Monoclonal antibody that targets HER2, so is used in HER2+ breast cancer, and is contraindicated during pregnancy
Trastuzumab
147
Trastuzumab is contraindicated in this
Pregnancy
