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 acute inflammation in irradiated tissues when chemotherapy is administered after radiation
A
Radiation recall
7
Q
Is this a reproductive toxicity of alkylating agents or methotrexate:
Multiple birth defects
A
Alkylating agents
8
Q
Is this a reproductive toxicity of alkylating agents or methotrexate:
Neural tube defects
A
Methotrexate
9
Q
What component of nucleosides (sugars and bases) can act as a nucleophile?
A
Both
10
Q
Outcome of treatment with alkylating agents that is less repairable/higher cytotoxicity
A
Irreversible crosslinking of two guanines (within and between chains)
11
Q
A less repairable/higher cytotoxic outcome of alkylating agents is the irreversible crosslinking of these
A
Two guanines
12
Q
Cisplatin, Carboplatin, Oxaliplatin, and Cyclophosphamide are this type of antineoplastic agent
A
Alkylating agents
13
Q
Cisplatin is this type of antineoplastic agent
A
Alkylating agent
14
Q
Carboplatin is this type of antineoplastic agent
A
Alkylating agent
15
Q
Cyclophosphamide is this type of antineoplastic agent
A
Alkylating agent
16
Q
Busulfan is this type of antineoplastic agent
A
Alkylating agent
17
Q
Primary toxicity of busulfan (an alkylating agent)
A
Pulmonary fibrosis (“Busulfan lung”)
18
Q
Carmustine, lomustine, and semustine are this type of neoplastic agent
A
Alkylating agents
19
Q
Alkylating agent with pulmonary fibrosis as a primary toxicity
A
Busulfan
20
Q
Primary toxicity of carmustine, lomustine, and semustine (alkylating agents)
A
Bone marrow depression that may be delayed and prolonged
21
Q
Alkylating agents with bone marrow depression that may be delayed and prolonged as a primary toxicity
A
Carmustine, lomustine, semustine
22
Q
2 primary toxicities associated with ciplastin, carboplatin, and oxaliplatin (alkylating agents)
A
Nephrotoxicity and Ototoxicity
23
Q
Alkylating agent that causes powerful nausea and vomiting
A
Cisplatin
24
Q
Primary toxicity of cisplatin (alkylating agent)
A
Powerful nausea and vomiting
(also nephrotoxicity and ototoxicity)
25
Nephrotoxicity and ototoxicity are toxicities associated with these alkylating agents
Cisplatin, carboplatin, oxaliplatin
26
2 Alkylating agents with toxicities involving hemorrhagic cystitis caused by acrolein (a CYP metabolite)
Cyclophosphamide, ifosfamide
27
Primary toxicity associated with cyclophosphamide and ifosfamide (alkylating agents)
Hemorrhagic cystitis
caused by acrolein (a CYP metabolite)
28
Hemorrhagic cystitis may be reduced in patients taking cyclophosphamide or ifosfamide with these
Mesna or amifostine (scavenger compound for acrolein)
29
CYP metabolite that causes hemorrhagic cystitis in patients taking cyclophosphamide or ifosfamide
Acrolein
30
Mesna or amifostine (scavenger compound for acrolein) reduces hemorrhagic cystitis and is required for this alkylating agent
Ifosfamide
31
Dacarbazine and mechlorethamine are alkylating agents with this effect
Vesicant (blistering agents)
32
Alkylating agent that uses phenylalanine transporter to enter cells (should be taken on an empty stomach)
Melphalan
33
Melphalan is an alkylating agent that uses this to enter cells
Phenylalanine transporter
34
Diabetes is a primary toxicity associated with this alkylating agent
Streptozocin
action is specific for beta cells of pancreas
35
Streptozocin is an alkylating agent with this primary toxicity
Diabetes
Action is specific for pancreas beta cells
36
Alkylating agent with risk of opportunistic infections, especially of the lungs
Temozolomide
37
Methotrexate, pemetrexed, and pralatrexate are this type of antimetabolite
Antifolates
38
6-mercaptopurine, Fludarabine, and Cladribine are this type of antimetabolite
Purine analogs
39
5-fluorouracil, capecitabine, cytarabine, azacitidine, and gemcitabine are this type of antimetabolite
Pyrimidine analogs
40
Methotrexate is this type of antineoplastic agent
Antifolate
41
6-Mercaptopurine is this type of antineoplastic agent
Purine analog (antimetabolite)
42
5-fluorouracil is this type of antineoplastic agent
Pyrimidine analog (antimetabolite)
43
Gemcitabine is this type of antineoplastic agent
Pyrimidine analog (antimetabolite)
44
Antifolates are specific for this cell cycle phase
S phase
45
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
46
MOA of methotrexate and pralatrexate
Inhibition of dihydrofolate reductase
47
Methotrexate inhibits this
Dihydrofolate reductase
48
2 antifolates that inhibit dihydrofolate reductase
Methotrexate and Pralatrexate
49
MOA of pemetrexed
Inhibition of dihydrofolate reductase and thymidylate synthase
50
Pemetrexed inhibits these 2 enzymes
Dihydrofolate reductase
Thymidylate synthase
51
Antimetabolite that inhibits dihydrofolate reductase and thymidylate synthase
Pemetrexed
52
Main toxicity of antifolates
Bone marrow depression
53
Bone marrow depression, neurotoxicity, and nephrotoxicity are toxicities of this type of antineoplastic agent
Antifolates
54
Reduced folate that uses the same entry mechanism as methotrexate
Leucovorin
55
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
56
Cancer cell resistance mechanism of antifolates prevents rescue by this
Leucovorin
57
Reduced folate that is used as a "rescue" for normal cells from high dose methotrexate while cancer cells die
Leucovorin
58
Leucovorin rescues normal cells from high doses of this antineoplastic agent while cancer cells die
Methotrexate (antifolate)
59
Purine analog whose dose should be reduced by 50-70% with concurrent use of allopurinol or febuxostat
6-Mercaptopurine
60
6-mercaptopurine is this type of anti-cancer agent
Purine analog
61
6-mercaptopurine dose should be reduced by 50-70% with concurrent use of either of these
Allopurinol or Febuxostat
62
Allopurinol and febuxostat are inhibitors of xanthine oxidase, which normally inactivates this purine analog
6-mercaptopurine
63
Allopurinol and Febuxostat are inhibitors of this enzyme which normally inactivates 6-mercaptopurine
Xanthine oxidase
64
Fludarabine is this type of anti-cancer agent
Purine analog
65
Toxicity of Fludarabine (purine analog)
Neurologic toxicity
66
Purine analog that is not for oral use; gut bacteria convert it to a toxic product
Fludarabine
67
Purine analog with neurologic toxicity
Fludarabine
68
Cladribine is this type of anti-cancer agent
Purine analog
69
Cladribine has this toxicity
Immunosuppression
and neurotoxicity
70
Purine analog with immunosuppression as a toxicity
Cladribine
71
Pyrimidine analogues inhibit DNA synthesis by blocking this enzyme
Thymidylate synthase
72
Pyrimidine analog with these toxicities:
Myelosuppression, coronary vasospasm, 'foot/hand' syndrome
5-Fluorouracil
73
5-Fluorouracil is this type of anti-cancer agent
Pyrimidine analog
74
Pyrimidine analog that is a powerful radiosensitizer (radiation recall)
Gemcitabine
75
Antibiotics with the suffix "-rubicin" have this toxicity
Intercalate with calcium channels --> Cardiotoxicity
76
Why do antibiotics with the suffix "-rubicin" cause cardiotoxicity?
Because they intercalate with calcium channels
77
Antibiotics for cancer that have cumulative lifetime limits
Daunorubicin, Doxorubicin, Epirubicin, Idarubicin
"-rubicin"
Due to cardiac toxicity
78
Cancer antibiotic with pulmonary fibrosis and mucocutaneous reactions as toxicities
Bleomycin
79
Primary toxicity of Bleomycin
Pulmonary fibrosis
"Bleomycin lung"
80
Bleomycin is inactivated by this
Hydrolase
Low activity in skin and lungs
81
This should be monitored in patients taking Bleomycin
Pulmonary function
82
Cardiac toxicity and radiation recall are toxicities of this cancer antibiotic
Daunorubicin
83
Cardiac toxicity with -rubicin use can be reduced by concurrent use of this
Iron chelator (dexrazoxane)
84
-rubicin concurrent use of iron chelator (dexrazosane) can reduce this
Cardiac toxicity
85
MOA of Vincristine, Vinblastine and Vinorelbine
Block formation of mitotic spindles by inhibition of polymerization
86
MOA of Paclitaxel and Docetaxel
Promote microtubule polymerization and stabilization, preventing their disassembly leading to accumulation of nonfunctional microtubules (mitosis freezes in metaphase)
87
3 drugs with this MOA:
Block formation of mitotic spindles by inhibition of polymerization
Vincristine, Vinblastine, Vinorelbine
88
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
89
3 microtubule inhibitors that are vesicants
Vincristine, Vinblastine, Vinorelbine
90
2 microtubule inhibitors with hypersensitivity reactions
Paclitaxel, Docetaxel
91
Microtubule inhibitor with neurotoxicity
Vincristine
92
Microtubule inhibitor with myelosuppression
Vinblastine
(also vinorelbine)
93
3 toxicities of Paclitaxel and Docetaxel
Myelosuppression, Neurotoxicity, Alopecia
94
Primary toxicity of Vincristine
Neurotoxicity
95
Primary toxicity of Vinblastine
Myelosuppression
96
2 S-phase specific inhibitors of topoisomerase I
Do not relieve torsional strain in DNA, leading to breaks
Irinotecan and Topotecan
97
MOA of Irinotecan and Topotecan
S-phase specific inhibitors of topoisomerase I
98
Irinotecan and Topotecan are S-phase specific inhibitors of this
Topoisomerase I
99
Topoisomerase inhibitor with life-threatening diarrhea as a toxicity
Responds well to atropine
Irinotecan
100
Primary toxicity of topotecan and etoposide
Bone marrow depression
101
Anticancer agent that is a S and G2-phase specific inhibitor of topoisomerase II
Etoposide
102
MOA of etoposide
S and G2-phase specific inhibitor of topoisomerase II
103
Target of Trastuzumab
Human epidermal growth factor receptor 2 (HER2)
104
Human epidermal growth factor receptor 2 (HER2) is a target for this monoclonal antibody
Trastuzumab
105
Cancer monoclonal antibody with increased risk of heart failure
Trastuzumab
106
Primary toxicity of Trastuzumab
Increased risk of heart failure
107
Target for Rituximab
CD20 antigen on normal and malignant B cells
108
CD20 antigen on normal and malignant B cells is the target of this monoclonal antibody
Rituximab
109
Bone marrow suppression is the primary toxicity of this monoclonal antibody
Rituximab
110
Primary toxicity of Rituximab
Bone marrow suppression
111
Target of Bevacizumab
Vascular endothelial growth factor (VEGF); inhibits angiogenesis
112
Vascular endothelial growth factor (VEGF) is the target of this monoclonal antibody
Bevacizumab
113
Target of Cetuximab
Blocks binding to the epidermal growth factor receptor on cancer cells
114
Monoclonal antibody that blocks binding to the epidermal growth factor receptor on cancer cells
Cetuximab
115
Acneiform-type rash is a primary toxicity of this monoclonal antibody
Cetuximab
116
Primary toxicity of Cetuximab
Aceniform-type rash
117
What is a positive sign of therapy of Cetuximab?
Aceniform-type rash
118
Drug names ending in "-nib" are inhibitors of this
Targeted kinase inhibitors
119
Drug names ending in "-nib" are toxic to this
Heart
(are targeted kinase inhibitors)
120
Targeted kinase inhibitors are often toxic to this
Heart
121
Targeted kinase inhibitor:
Rash is common and typically related to stronger therapeutic responses
Erlotinib
122
Targeted kinase inhibitor where you should monitor for signs of heart failure and wound-healing complications
Sorafenib
123
This is a common side effect of Erlotinib and is typically related to stronger therapeutic responses
Rash
124
Primary toxicity of Erlotinib
Rash
125
Mechlorethamine + Oncovin/Vincristine + Prednisone + Procarbazine ("MOPP") is a combination therapy indicated for this
Hodgkin's lymphoma
126
Melanoma changes with this mutation
BRAF mutation
127
Cancer that changes with BRAF mutation
Melanoma
128
Breast cancer therapy for ER+/PR+ in premenopause
Tamoxifen
129
ER antagonist in breast; indicated for breast cancer that expresses ER (ER+)
Tamoxifen
130
Breast cancer therapy for ER+/PR+ in postmenopause
Aromatase inhibitors
131
Drugs that 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
132
Breast cancer therapy for ER-/PR-/HER2+
Trastuzumab and/or lapatinib, +/- chemotherapy
133
Breast cancer therapy for ER-/PR-/HER2-
Chemotherapy
Anthracycline + cyclophosphamide +/- taxane
134
Tamoxifen or Aromatase inhibitors are treatment for this type of breast cancer
ER+/PR+
135
Trastuzumab and/or lapatinib, +/- chemotherapy, is treatment for this type of breast cancer
ER-/PR-/HER2+
136
Chemotherapy (Anthracycline + cyclophosphamide +/- taxane) is treatment for this type of breast cancer
ER-/PR-/HER2- (TNBC)
137
Monoclonal antibody that targets HER2, so is used in HER2+ breast cancer, and is contraindicated during pregnancy
Trastuzumab
138
Trastuzumab is contraindicated in this
Pregnancy
