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PHRM864 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What are the hallmarks of cancer?

A

-sustaining proliferative staging
-avoiding immune destruction
-enabling replicative immortality
-activating invasion and metastasis
-inducing or accessing vasculature
-genome instability and mutation
-resisting cell death

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2
Q

What are the characteristics of cancer?

A

-uncontrolled cellular growth
-invasion of tissue
-metastasis

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3
Q

neoplasm

A

a new growth; may be benign or malignant

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4
Q

tumor

A

a lump or swelling; may be benign or malignant

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5
Q

cancer

A

any malignant neoplasm

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6
Q

hyperplasia

A

an increase in organ or tissue size due to an increase in the number of cells; can be physiologic, compensatory, or pathologic

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7
Q

metaplasia

A

an adaptive substitution of one type of adult tissue to another type of adult tissue

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8
Q

dysplasia

A

an abnormal cellular proliferation in which loss of normal architecture occurs

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9
Q

anaplasia

A

a loss of structural differentiation

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10
Q

carcinoma

A

malignant neoplasm of squamous epithelial cell origin

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11
Q

adenocarcinoma

A

malignant neoplasm derived from glandular tissue

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12
Q

sarcoma

A

malignant neoplasm with origin in mesenchymal tissues or its derivatives

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13
Q

lymphoma and leukemia

A

malignant neoplasms of hematopoietic tissues

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14
Q

melanoma

A

a type of cancer of pigment-producing cells (melanocytes) in the skin or eye (uveal melanoma)

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15
Q

blastoma

A

malignancies in precursor cells

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16
Q

teratoma

A

a germ cell neoplasm made of several different differentiated cell/tissue types

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17
Q

Is p53 an oncogene or tumor suppressor?

A

tumor suppressor

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18
Q

Is p16 an oncogene or tumor suppressor?

A

tumor suppressor

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19
Q

Is Ras an oncogene or tumor suppressor?

A

oncogene

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20
Q

Is Rbl an oncogene or tumor suppressor?

A

tumor suppressor

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21
Q

What is a limitation of phase-specific drugs?

A

number of cells in specific phase at that time

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22
Q

What are dose-limiting toxicities of chemotherapy?

A

-infections
-hemostasis
-anemia
-GI side effects
-N/V
-loss of appetite

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23
Q

What are mechanisms of drug resistance for chemotherapy?

A

-altered drug metabolism
-changes in drug target or function
-physiological changes
-cell survival mechanisms

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24
Q

How can drug metabolism be altered?

A

-increased transport of drugs out of cell through efflux pumps
-reduced transport into cell
-decreased activation of prodrug
-increased detoxification of drug molecule

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25
Q

How can drug target or function be changed?

A

-increased expression of drug target through gene amplification or expression
-emergence of structurally mutated target
-rewire pathway to bypass need for drug target

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26
Q

What are physiological changes that can lead to drug resistance for chemotherapy?

A

-refuge of cancer cells in drug-protected anatomical sites
-massive stromalization
-changes in cell state

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27
Q

What are cell survival mechanisms?

A

-activation of anti-apoptotic regulators
-increased repair of damage caused by chemotherapies

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28
Q

What is the suffix of androgen receptor antagonists?

A

-lutamide

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29
Q

What are the mechanisms of action of androgen receptor antagonists?

A

-prevent androgen receptor translocation to nucleus
-inhibits androgen receptor binding to DNA

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30
Q

What is the indication of androgen receptor antagonists?

A

metastatic and non-metastatic prostate cancer

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31
Q

What is the mechanism of action of abiraterone?

A

inhibits function of 17α-hydroylase and 17,20 lyase

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32
Q

What is the function of 17α-hydroylase and 17,20 lyase?

A

convert progestogens to androgens

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33
Q

What is a common side effect of abiraterone?

A

increased cholesterol

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34
Q

What type of drug is tamoxifen?

A

selective estrogen receptor modulator (SERM) prodrug

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35
Q

Does tamoxifen have agonist or antagonist activities?

A

agonist and antagonist

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36
Q

What are tamoxifen antagonist effects?

A

-blocks estrogen-dependent breast cancer cell proliferation
-hot flashes

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37
Q

What are tamoxifen agonist effects?

A

-increased incidence of endometrial cancer
-preservation of bone density in postmenopausal women

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38
Q

What population is tamoxifen effective in?

A

pre- and post-menopausal women

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39
Q

What are the indications for tamoxifen?

A

resected and metastatic ER+/PR+ breast cancer

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40
Q

What is the recommended duration of use for tamoxifen?

A

up to 5 years

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41
Q

What type of drug is fulvestrant?

A

selective estrogen receptor down-modulator (SERD)

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42
Q

Does fulvestrant have agonist or antagonist activities?

A

antagonist

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43
Q

What is the mechanism of action of fulvestrant?

A

binds to estrogen receptor and inhibits DNA binding –> rapid receptor degradation

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44
Q

What is the indication of fulvestrant?

A

ER+ metastatic breast cancer in postmenopausal women who have progressed on other anti-estrogen therapy

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45
Q

What is the route of administration of fulvestrant?

A

IM

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46
Q

What cancers do glucocorticoids have anti-cancer effects in?

A

-pediatric acute lymphoblastic leukemia
-multiple myeloma
-lymphoma

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47
Q

What are the most commonly used glucocorticoids in cancer treatment?

A

-methylprednisolone
-prednisolone
-dexamethasone

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48
Q

What is the suffix of non-steroidal aromatase inhibitors?

A

-trozole

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49
Q

Are non-steroidal aromatase inhibitors competitive or non-competitive?

A

competitive

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50
Q

What is the indication of non-steroidal aromatase inhibitors?

A

breast cancer in postmenopausal women

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51
Q

When should non-steroidal aromatase inhibitors be used in treatment?

A

first-line OR after 3-5 years of tamoxifen treatment

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52
Q

What is a side effect of non-steroidal aromatase inhibitors?

A

increased bone density loss

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53
Q

What are the two steroidal aromatase inhibitor drugs?

A

-exemestane
-androstenedione

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54
Q

What is the mechanism of action of exemestane?

A

-false substrate that aromatase converts to reactive intermediate
-intermediate binds irreversibly at active site and inactivates enzyme

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55
Q

What is the indication of exemestane?

A

ER+ breast cancer in postmenopausal women who have progressed on anti-estrogen therapy

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56
Q

What are side effects of exemestane?

A

-hot flashes
-occasional peripheral edema and weight gain
-increased cholesterol

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57
Q

What is the function of aromatase?

A

convert androgens to estrogens

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58
Q

What are two GnRH analogs?

A

-leuprolide
-goserelin

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59
Q

What are long-term side effects of GnRH analogs?

A

-hot flashes
-gynecomastia
-sexual dysfunction

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60
Q

What are the indications of GnRH analogs?

A

-premenopausal breast cancer
-palliative treatment of advanced prostate cancer

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61
Q

What is a clinical pearl of GnRH analogs?

A

temporary worsening of symptoms due to initial agonist effects

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62
Q

What drugs are given to premenopausal women with breast cancer?

A

-GnRH analogs
-tamoxifen

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63
Q

What drugs are given to postmenopausal women with breast cancer?

A

-tamoxifen
-aromatase inhibitors
-SERDs

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64
Q

What is the suffix of kinase inhibitors?

A

-nib

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65
Q

What is the mechanism of action of imatinib?

A

type II small molecule inhibitor of Abl tyrosine kinase

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66
Q

What is the mechanism of action of type II kinase inhibitors?

A

bind and stabilize inactive conformation of kinase

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67
Q

What is the indication of imatinib?

A

chronic myeloid leukemia (CML)

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68
Q

What are side effects of imatinib?

A

-N/V
-fluid retention and edema
-neutropenia and thrombocytopenia

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69
Q

What is the mechanism of action of ponatinib?

A

BCR-Abl inhibitor

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70
Q

What mutation can ponatinib inhibit that other BCR-Abl inhibitors cannot?

A

T315I

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71
Q

What is the mechanism of action of type I kinase inhibitors?

A

bind to active conformation of kinase

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72
Q

What type of FLT3 inhibitor is midostaurin?

A

first generation

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73
Q

Are first generation FLT3 inhibitors more broad or specific?

A

broad

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74
Q

What drugs are type I FLT3 inhibitors?

A

-midostaurin
-crenolanib

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75
Q

What is the indication of FLT3 inhibitors?

A

acute myeloid leukemia (AML)

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76
Q

What drug is a type II FLT3 inhibitor?

A

-quizartinib

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77
Q

What mutation are type II FLT3 inhibitors specific for?

A

internal tandem duplication (ITD)

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78
Q

What type of FLT3 inhibitor is crenolanib?

A

second generation

79
Q

Are second generation FLT3 inhibitors more broad or specific?

A

specific

80
Q

What is the suffix of rapamycin analogs?

A

-rolimus

81
Q

What do rapamycin analogs inhibit the function of?

A

mTOR

82
Q

What is the mechanism of action of rapamycin analogs?

A

inhibit immune response by blocking IL-2 signaling transduction

83
Q

What is the indication of everolimus?

A

advanced renal carcinoma in patients who have failed sunitinib or sorafenib

84
Q

Does everolimus inhibitor mTORC1 or mTORC2?

A

mTORC1

85
Q

What is the mechanism of action of alectinib?

A

specific inhibitor of ALK

86
Q

What does alectinib require before prescribing?

A

companion diagnostic test for fusion gene

87
Q

What is the indication of alectinib?

A

ALK+ metastatic non-small cell lung cancer (NSCLC) with progression or intolerance to crizotinib

88
Q

What is the mechanism of action of dabrafenib?

A

second generation BRAF-V600 inhibitor

89
Q

What are the indications of dabrafenib?

A

-BRAF V600E/K-mutant metastatic melanoma
-BRAF-600+ NSCLC

90
Q

What is the mechanism of action of trametinib?

A

inhibits kinase activity of MEK1 and MEK2

91
Q

What type of kinase inhibitor is trametinib?

A

type III

92
Q

What is the mechanism of action of type III kinase inhibitors?

A

occupy allosteric pocket outside ATP-binding pocket

93
Q

What are side effects of trametinib?

A

-rash
-diarrhea
-lymphedema

94
Q

What is the mechanism of action of acalabrutinib?

A

second generation covalent BTK inhibitor

95
Q

What is the indication of acalabrutinib?

A

B-cell lymphoma

96
Q

What are the EGFR inhibitor drugs?

A

-gefitinib
-afatinib
-osimertinib

97
Q

What is the indication of gefitinib and afatinib?

A

metastatic NSCLC with EGFR exon 19 or 21 mutations

98
Q

What are the side effects of gefitinib?

A

-fatigue
-rash
-diarrhea

99
Q

What mutation is osimertinib effective against?

A

T790M

100
Q

What is the mechanism of action of lapatinib?

A

reversible small molecule tyrosine kinase inhibitor blocking HER2 and EGFR signaling

101
Q

What is the indication of lapatinib?

A

advanced metastatic cancer progressive on other therapies

102
Q

What are side effects of lapatinib?

A

-diarrhea
-N/V
-reversible decrease in cardiac function

103
Q

What is the mechanism of action of tucatinib?

A

small molecule tyrosine kinase inhibitor that preferentially binds HER2

104
Q

What is the indication of tucatinib?

A

second-line treatment for advanced metastatic breast cancer progressive on other therapies

105
Q

Which EGFR inhibitors bind covalently?

A

-afatinib
-osimertinib

106
Q

What part of the cell cycle do antimetabolites target?

A

S phase

107
Q

What is a dose-limiting toxicity of antimetabolites?

A

myelosuppression

108
Q

What drugs are pyrimidine analogs?

A

-5-FU
-capecitabine

109
Q

What are the mechanisms of action of 5-FU?

A

-conversion to FdUMP mimics dUMP –> TMP cannot be produced –> inhibition of DNA synthesis
-conversion to F-UTP –> fluorine interferes with RNA processing and function and with polyadenylation of mRNA

110
Q

What drug is used as a rescue for 5-FU?

A

thymidine

111
Q

What are resistance mechanisms of 5-FU?

A

-downregulation of activating enzymes that convert 5-FU to FdUMP
-upregulation of thymidylate synthaseW

112
Q

What polymorphism increases susceptibility to 5-FU?

A

DPD

113
Q

What drug is used synergistically with 5-FU?

A

leucovorin

114
Q

What drugs are cytidine analogs?

A

-cytarabine (Ara-C)
-gemcitabine

115
Q

What is the mechanism of action of cytarabine?

A

-converted to Ara-CTP intracellularly
-competitive inhibitor of DNA polymerase α

116
Q

What cancer is cytarabine best at targeting?

A

meningeal leukemia and lymphoma

117
Q

What are resistance mechanisms of cytarabine?

A

-downregulation of activating enzymes and transporter to move drug into cell
-upregulation of cytidine deaminase

118
Q

What drug is used synergistically with cytarabine?

A

tetrahydrouridine

119
Q

How is gemcitabine more beneficial than cytarabine?

A

higher potency

120
Q

What drugs are purine analogs?

A

-6-mercaptopurine
-6-thioguanine

121
Q

What is a resistance mechanism of 6-mercaptopurine?

A

loss of HGPRT

122
Q

What polymorphism causes increased toxicity of 6-mercaptopurine?

A

TPMT

123
Q

What is a drug interaction with 6-mercaptopurine but not 6-thioguanine?

A

allopurinol

124
Q

What drug is an antifolate?

A

methotrexate

125
Q

What is the mechanism of action of methotrexate?

A

DHFR inhibitor

126
Q

What are resistance mechanisms of methotrexate?

A

-amplification of DHFR gene or mutation of DHFR to resistant form
-decreased polyglutamation

127
Q

What is a side effect of methotrexate?

A

myelosuppression

128
Q

What drug is used as a rescue for methotrexate?

A

leucovorin

129
Q

What are side effects of alkylating agents?

A

-myelosuppression
-N/V

130
Q

What drug class is chlorambucil in?

A

mechlorethamine derivatives

131
Q

How are mechlorethamine derivatives more beneficial than mechlorethamine?

A

reduced reactivity and increased selectivity of nitrogen mustards

132
Q

Are alkylating agents cell cycle phase specific?

A

No

133
Q

What type of drug is cyclophosphamide?

A

prodrug alkylating agent

134
Q

What are side effects of cyclophosphamide?

A

-bone marrow toxicity
-hemorrhagic cystitis

135
Q

What drug is administered with cyclophosphamide to prevent hemorrhagic cystitis?

A

mesna

136
Q

What type of drug is mitomycin C?

A

alkylating agent

137
Q

What is a dose-limiting side effect of mitomycin C?

A

myelosuppression

138
Q

What is the suffix of platinum drugs?

A

-platin

139
Q

What is the mechanism of action of platinum drugs?

A

covalent crosslinkers

140
Q

What type of crosslinks are formed by platinum drugs?

A

intrastrand

141
Q

What type of tumors are platinum drugs highly effective for?

A

solid tumors

142
Q

What are side effects of cisplatin?

A

-N/V
-bone marrow toxicity
-peripheral neuropathy
-ototoxicity

143
Q

What is a dose-limiting side effect of cisplatin?

A

nephrotoxicity

144
Q

What are resistance mechanisms of alkylating agents and platinum drugs?

A

-increased expression of DNA repair enzymes
-increased intracellular concentration of non-protein thiones
-increased expression of cellular glutathione S-transferase (GST)

145
Q

What phase of the cell cycle are cells most susceptible to topoisomerase I inhibitors?

A

S phase

146
Q

What are resistance mechanisms of topoisomerase I and II inhibitors?

A

-PGP overexpression
-MRP overexpression
-glutathione S-transferase overexpression
-topoisomerase downregulation or mutation

147
Q

What is the suffix of camptothecins?

A

-otecan

148
Q

What polymorphism causes increased toxicity of irinotecan?

A

UGT1A1

149
Q

How many strands of DNA does topoisomerase I cut?

A

one

150
Q

How many strands of DNA dose topoisomerase II cut?

A

two

151
Q

Are topoisomerase II inhibitors cell cycle phase specific?

A

No

152
Q

What cell cycle phase do topoisomerase II inhibitors have greater activity in?

A

G2/M

153
Q

What is the suffix of anthracyclines?

A

-rubicin

154
Q

What are side effects of doxorubicin?

A

-cardiotoxicity
-local tissue damage

155
Q

What drug mediates cardiotoxicity associated with anthracyclines?

A

dexrazoxane

156
Q

How is etoposide different than anthracyclines?

A

not an intercalator

157
Q

What cell cycle phase does etoposide target?

A

G2

158
Q

What is a resistance mechanism for topoisomerase II inhibitors?

A

increased DNA damage repair

159
Q

What cell cycle phases does bleomycin target?

A

G2/M

160
Q

What is a side effect of bleomycin?

A

myelosuppression

161
Q

What is a dose-limiting side effect of bleomycin?

A

pulmonary side effects

162
Q

What is the mechanism of action of vinka alkaloids?

A

prevent microtubule assembly

163
Q

What is the mechanism of action of taxanes?

A

prevent microtubule disassembly

164
Q

What is a side effect of vinka alkaloids?

A

peripheral neuropathy

165
Q

What are side effects of vincristine?

A

-local inflammation
-myleosuppression

166
Q

What is a dose-limiting side effect of vincristine?

A

neurotoxicity

167
Q

How is eribulin beneficial compared to vincristine?

A

lower rate of neurotoxicity

168
Q

What is the suffix of taxanes?

A

-taxel

169
Q

What is a side effect of paclitaxel?

A

neurotoxicity

170
Q

What is a dose-limiting side effect of paclitaxel?

A

myelosuppression

171
Q

What is a clinical pearl of ixabepilone?

A

not cross-resistant with taxanes

172
Q

What is the mechanism of action of pembrolizumab?

A

PD-1 inhibitor

173
Q

What are the indications for pembrolizumab?

A

-advanced metastatic melanoma after treatment with ipilimumab and BRAF inhibitor
-PD-L1+ NSCLC

174
Q

What is the mechanism of action of atezolizumab?

A

PD-L1 inhibitor

175
Q

What is the mechanism of action of ipilimumab?

A

binds to CTLA-4 receptor and reverses CTL inhibition

176
Q

What is the indication of ipilimumab?

A

advanced metastatic melanoma

177
Q

What are side effects of ipilimumab?

A

-enterocolitis
-hepatitis
-dermatitis
-neuropathy
-endocrinopathy

178
Q

What is the mechanism of action of trastuzumab and pertuzumab?

A

recombinant humanized monoclonal antibody specific for HER2

179
Q

What is the indication of trastuzumab?

A

HER2+ breast cancer

180
Q

What are side effects of trastuzumab?

A

-flu-like symptoms
-risk of cardiomyopathy/CHF
-risk of hypersensitivity reactions

181
Q

What region of HER2 does trastuzumab bind to?

A

region IV

182
Q

What region of HER2 does pertuzumab bind to?

A

region II

183
Q

What is the mechanism of action of cetuximab?

A

recombinant chimeric monoclonal antibody specific for EGFR

184
Q

What are the indications of cetuximab?

A

-colorectal cancer
-head and neck cancer

185
Q

What are side effects of cetuximab?

A

-infusion reaction
-acneiform rash
-fatigue
-fever

186
Q

What is the mechanism of action of bevacizumab?

A

recombinant humanized monoclonal antibody specific for VEGF

187
Q

What is the indication of bevacizumab?

A

metastatic colorectal cancer in combination with 5-FU

188
Q

What does bevacizumab bind?

A

VEGF ligand

189
Q

What does ramucirumab bind?

A

VEGF receptor

190
Q

What is the mechanism of action of rituximab?

A

CD20 antibody

191
Q

What is the indication of rituximab?

A

B-cell lymphomas

192
Q

What is the mechanism of action of daratumumab?

A

CD38 antibody

193
Q

What is the indication of daratumumab?

A

multiple myeloma

PHRM864 (6 decks)

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