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Heme Path Exam 1 > INTRODUCTION TO ANTINEOPLASTIC AGENTS > Flashcards

INTRODUCTION TO ANTINEOPLASTIC AGENTS Flashcards

1
Q

Top10 Cancer Sites
Estimated NewCases 2015
EstimatedDeaths 2015

A 
1.
Breast Cancer (Female)
231,840
40,290
2.
Lung and Bronchus Cancer
221,200
158,040
3.
ProstateCancer
220,800
27,540
4.
Colon and Rectum Cancer
132,700
49,700
5.
Bladder Cancer
74,000
16,000
6.
Melanoma of the Skin
73,870
9,940
7.
Non-Hodgkin Lymphoma
71,850
19,790
8.
Thyroid Cancer
62,450
1,950
9.
Kidney and Renal Pelvis Cancer
61,560
14,080
10.
Endometrial Cancer
54,870
10,170
All Cancer Sites
1,658,370
589,430
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2
Q

Alkylating Agents

nitrogen mustards

A

cyclophosphamide

ifosfamide

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3
Q

Alkylating Agents

alkyl sulfonate

A

busulfan

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4
Q

Alkylating Agents

platinum coordination complexes

A

cisplatin

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5
Q

Natural Products

vinca alkaloids

A

vinblastine

vincristine

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6
Q

Natural Products

taxanes

A

paclitaxel

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7
Q

Natural Products

epipodophyliotoxins

A

etoposide

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8
Q

Natural Products

antibiotics

A

bleomycin

doxorubicin

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9
Q

Natural Products

eznymes

A

l asparaginase

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10
Q

Antimetabolites

folic acid analogs

A

methotrexate

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11
Q

Antimetabolites

pyrimidine analogs

A

fluorouracil

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12
Q

Antimetabolites

purine analogs

A

mercaptopurine

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13
Q

Differentiating agents

A

tretinoin

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14
Q

biological response modifiers

A

Interferon-alfa

Interleukin-2

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15
Q

Immunomodulators

A

Thalidomide

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16
Q

Rescue agents

A
  • Leucovorin

* Mesna

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17
Q

Protein tyrosine kinase inhibitors

A

dasatinib

erlotinib

imatinib

lapatinib

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18
Q

proteasome inhibitors

A

bortezomib

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19
Q

monoclonal abs

A

bevacizumab

cetuximab

rituximab

trastuzumab

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20
Q

Agents used to minimize adverse effects

A

erythropoietin

filgrastim

ondandetron - serotonin antagonists

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21
Q

Cancer Treatment Modalities

A
  • Chemotherapy
  • Immunotherapy
  • Radiation Therapy
  • Surgery
  • Targeted Therapies
  • Transplantation
  • Vaccines
  • Combinations are the norm
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22
Q

Primary Induction Therapy

A
  • The main treatment that provides the best possible outcome

* Also called first-line therapy

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23
Q

NeoadjuvantTherapy

A
  • Treatment given BEFORE primary induction therapy in order to improve outcome
  • E.g., Chemo or radiation to shrink a tumor before surgery
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24
Q

Adjuvant Therapy

A

•Additional therapy given CONCOMITANTLY or AFTER primary induction therapy in order to reduce the probability of relapse

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25
Q

g0 phase

A

resting

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26
Q

m phase

A

mitosis

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27
Q

g1 phase

A

synthesis of components needed of dna synthesis

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28
Q

s phase

A

synthesis of dna

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29
Q

g2 phase

A

synthesis of componeneint needed fo ritosis

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30
Q

cell phases in order

A 
g0
g1
s
g2
m
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31
Q

checpoints for dna

A

after g1

befro s phase finishes

end of g2

before m phase finishes

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32
Q

Cycling Out of Control

A
  • In many forms of cancer, proteins orpathways involved in regulating the checkpoints between the phases of the cell cycle may be absent or mutated
  • For example: p53, CDKs
  • Aberrations in checkpoint regulation result in uncontrolled and unregulated cell proliferation
  • Cell cycle specific vs. cell cycle nonspecific
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33
Q

Antimetabolites (S phase)

A

5-fluorouracil
6-mercaptopurine
Methotrexate

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34
Q

Antitumor antibiotics (S-G2phase)

A

bleomycin

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35
Q

Taxanes(M phase)

A

Paclitaxel

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36
Q

Vincaalkaloids (M phase)

A

Vinblastine

Vincristine

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37
Q

Topoisomerase II Inhibitors (Epipodophyllotoxins, S-G2 phase

A

Etoposide

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38
Q

Cell cycle nonspecific agents

Alkylating agents

A

Cyclophosphamide

Ifosphamide

Busulfan

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39
Q

Cell cycle nonspecific agents

Anthracyclines

A

Doxorubicin

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40
Q

Cell cycle nonspecific agents

Platinum analogs

A

Cisplatin

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41
Q

Growth Fraction and Tumor Growth Rate

A
  • Growth fraction = the ratio of proliferating cells to resting cells (G0)
  • Growth fraction is a determinant of responsiveness to chemotherapy
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42
Q

Cells with high growth fraction

A
  • Bone marrow
  • GI tract
  • Hair follicles
  • Sperm-forming cells
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43
Q

higher growth fraction =

A

shorter doubling time

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44
Q

lower growth fraction =

A

longer doubling time

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45
Q

Growth Fraction and Therapeutic Response

A
  • The initial growth rate of most solid tumors is rapid but decreases over time
  • Burkittlymphoma (high growth fraction; curable by chemotherapy) vs. colorectal carcinoma (low growth fraction; chemotherapy has minor activity)
  • Some disseminated tumors can be cured by single-agent chemotherapy
  • The growth fraction of solid tumors can be increased by reducing the tumor burden (i.e., surgery or radiation)
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46
Q

Log Cell Kill Hypothesis

A
  • A fraction (not an absolute number) of cells are killed
  • A three-log cell kill eliminates 99.9% of cells:
  • 1012to 109cells
  • 106to 103cells
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47
Q

Therapeutic Balance: Efficacy vs. Toxicity

•Challenge:

A

provide dose that is therapeutic without being (too) toxic
•Antineoplastic drugs harm both cancerous tissues and healthy tissues
•Not all drug regimens are appropriate for all patients

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48
Q

Therapeutic Balance: Efficacy vs. Toxicity

•Factors to consider:

A
  • Renal and hepatic function
  • Bone marrow reserve
  • General performance status
  • Concurrent medical problems
  • Patient willingness
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49
Q

Primary resistance

A
  • An absence of response on the first drug exposure

* Thought to be due to genomic instability

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50
Q

Acquired resistance

A
  • Develops in response to exposure to a given antineoplastic agent
  • Often highly specific to a single drug, or class of drugs, and is usually due to an increased expression of one or more genes
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51
Q

Examples of single agent resistance pathways include:

A
  • decreased drug transport into cells
  • reduced drug affinity due to mutations or alterations of the drug target
  • increased expression of an enzyme that causes drug inactivation
  • increased expression of DNA repair enzymes for drugs that damage DNA
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52
Q

Multidrug resistance and ATP-dependent Transporters

mechanism

A
  • ATP-dependent transporter gene amplification in neoplasms confers resistance to a broad range of agents used in cancer treatments
  • The P-glycoprotein is an ATP-dependent efflux pump that actively pumps antineoplastic agents out of cells (MDR1gene)
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53
Q

Multidrug resistance and ATP-dependent Transporters

drugs

A

Anthracyclines, vincaalkaloids, etoposide, paclitaxel, and dactinomycin

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54
Q

Toxicity of Antineoplastic Agents

A
  • The lack of neoplastic specificity for chemotherapeutic drugs is a major limiting factor in the treatment of cancer
  • Rapidly proliferating normal tissues (tissues with high growth fractions) are the major sites of toxicity
  • bone marrow, gastrointestinal tract, hair follicles, buccalmucosa, sperm forming cells
  • Many antineoplastic agents are mutagens themselves and can give rise to neoplasms years after treatment (e.g., alkylating agents have caused AML and ALL)
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55
Q

Common Adverse Effects

A
  • Nausea
  • Vomiting
  • Fatigue
  • Stomatitis
  • Alopecia
  • Myelosuppression –can lead to impaired wound healing and predisposition to infection
  • Low sperm counts and azoospermia
  • Depressed development of children exposed to antineoplastic agents
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56
Q
  • Nausea
  • Vomiting
  • Fatigue
  • Stomatitis
  • Alopecia
A

Occur during therapy with nearly all classicantineoplastic agents

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57
Q

Minimizing Adverse Effects

A
  • Choose the route of administration that minimizes systemic toxicity as much as possible
  • Pharmacologic agents that help decrease adverse effects
    • Hematopoietic agents for neutropenia, thrombocytopenia, and anemia
    • Serotonin receptor antagonist (ondansetron) and other drugs for emetogeniceffects
    • Bisphosphonates to delay skeletal complications
  • Rest and recovery
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58
Q

inhibit purine ring biosynthesis

inhibit dna synthesis

A

6 mercaptopurine

6 thiglianine

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59
Q

inhibit dihydrofolate reduction, block thymidylate and purine synthesis

A

alimta

methotrexate

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60
Q

block topoisomerase function

A 
camptothecins
etoposide
teniposide
dalincrubicin
doxorubicin
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61
Q

block activites of signaling pathways

A

protein tyrosine kinase inhibitors

antibodies

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62
Q

inhibits ribonucleoside reductase

A

hydroxyurea

63
Q

inhibits thymidylase synthesis

A

5 flurouracil

64
Q

inhibits dna synthesis

A 
gemcitabine
cytarabine
fludarabine
2-chlorodeoxyadenosine
clofarabine
65
Q

form adducts with dna

A

platinum analogs
alkylating agents
mitomycin
temozoloide

66
Q

deaminates asparagine

inhibits protein synthesis

A

l-asparaginase

67
Q

inhibit function of microtubules

A

epothilones
taxanes
vinca alkaloids
estramustine

68
Q

inducers of differntiation

A

atra
arsenic trioxide
histone deacelyase inhibitors

69
Q

what acts in m phase

A

mitotic inhibitors

70
Q

what acts in g2 phase

A

bleomycin etoposie and teniposide

71
Q

what acts in s phase

A

dna synthesis inhibitors

72
Q

what acts in no the cell cycle

A

all dna alkylating drugs and most dna intercalating agents

73
Q

Five major types of alkylating agents

A

1.Nitrogen mustards (cyclophosphamide)
2.Nitrosoureas(carmustine)
3.Alkyl sulfonates(busulfan)
4.Methylhydrazinederivatives (procarbazine)
5.Triazines(dacarbazine)
•Also included are platinum compounds (cisplatin)

74
Q

The nitrogen mustard cyclophosphamide is the most

A

widely used alkylating agent and one of the most emetogenicagents

75
Q

alkylating agents are cell cycle

A

nonspecific

76
Q

Alkylating Agents: Mechanism of Action

A

Alkylating agents form covalent linkages with DNA

intrastrand and cross-linking

77
Q

Biotransformation of Cyclophosphamide

A

goes to 4 hydroxyphosphamide that is either turned to inactive 4 ketocyclophasophamide by and enzyme or aldophosphamide by cype2b from here it is either inactivated by hepatic aldehyde oxidase to carboxyphosphamide or turned to phosphoramide mustard which is cytotoxic and acrolein which is also cytotoxis (mesna deactivates this one)

78
Q

Acroleincauses

A

hemmorhagic cystitis

79
Q

mesna

A

Mesnainactivates acroleinand is used for prophylaxis of chemotherapy-induced cystitis

80
Q

Alkylating Agents: Toxicities

overview

A
  • Systemic toxicities are dose related
  • Direct vesicant effects and tissue damage at site of injection (oral administration is of great clinical benefit)
  • Many alkylating agents produce acute toxicity, such as nausea and vomiting within 30-60 minutes (pretreat with serotonin antagonist)
  • Delayed toxicities include the common side effects of antineoplastics: bone marrow depression with leukopenia, thrombocytopenia, nephrotoxicity, alopecia, mucosal ulceration, intestinal denudation
81
Q

Cyclophosphamide ae

A

hemorrhagic cystitis

82
Q

Cisplatin ae

A

renal tubular damage ototoxicity

83
Q

busulfan ae

A

pulmonary fibrosi

84
Q

Three major types of antimetabolites

A
  1. Folic acid analogs (methotrexate)
  2. Pyrimidine analogs (5-Fluorouracil)
  3. Purine analogs (6-mercaptopurine)
85
Q

antimetabolites moa

A
  • Structural analogs to compounds necessary for cell proliferation
  • Block or subvert pathways that are involved in, or lead to, cell replication (nucleotide and nucleic acid synthesis)
86
Q

antimetabolites are cell cycle specific for what phase

A

s

87
Q

Methotrexate is a

A

folic acid analog

88
Q

methotrexate moa

A

•Inhibits dihydrofolatereductase(DHFR)

so dihydrofolic acid cant become tetrhydrofolic acid

89
Q

methotrexate indications

A
  • Cancer
  • Rheumatoid arthritis
  • Psoriasis
90
Q

Methotrexate & LeucovorinRescue

A
  • Leucovorin: reduced folatecan bypass DHFR
  • Used to rescue normal cells from high-dose MTX
  • Antidote for accidental MTX overdose

enters the cycle after methotrexate does its job

91
Q

cut the? into single pieces

A

pyrimidines,

92
Q

Pyrimidine Structural Analogs

A
  • Prototype: 5-Fluorouracil (5-FU)

* Prodrug

93
Q

Fluorouracil: Mechanisms of Action

Active compound (FdUMP)

A

covalently binds thymidylatesynthetaseand blocks de novosynthesis of thymidylate

94
Q

Fluorouracil: Mechanisms of Action

Active compounds (FdUTPand FUTP)

A

are incorporated into both DNA and RNA, respectively

95
Q

can leucovorin resue fluorouracil

A

no

96
Q

Purine Structural Analogs

A
  • Prototype: 6-Mercaptopurine (6-MP)

* Prodrug

97
Q

Purine Structural Analogs moa

A
  • Inhibition of several enzymes of de novopurine nucleotide synthesis
  • Incorporates into DNA and RNA
98
Q

Drug Interaction: 6-MP & Allopurinol

A
  • Biotransformation of 6-MP includes metabolism to the inactive metabolite 6-thiouric acid by xanthine oxidase (first pass effect)
  • Allopurinol, a xanthine oxidase inhibitor, is often used as supportive care in the treatment of acute leukemiasto prevent hyperuricemiadue to tumor cell lysis
  • Simultaneous administration of allopurinol and oral6-MP results in increased levels of 6-MP and increased toxicity
  • Reduce oral 6-MP dose by 50-75%; IV dose unaffected
99
Q

Antimetabolites: Pharmacodynamics

A
  • Cell cycle specific (S-phase)
  • Relatively little acute toxicity after an initial dose
  • Oral, intravenous, intrathecal(methotrexate) are common routes of administration
100
Q

antimetabolites common toxicities

A

diarrhea, myelosuppression, nausea, vomiting, immunosuppression, thrombocytopenia, leukopenia, hepatotoxicity

101
Q

VincaAlkaloids drugs

A

vinblastineand vincristine

102
Q

VincaAlkaloids adverse effects

A
  • Alopecia
  • Myelosuppression(vinblastine > vincristine)
  • Vincristine exhibits neurotoxicity (numbness and tingling of the extremities, loss of deep tendon reflexes, motor weakness, autonomic dysfunction has also been observed)
103
Q

VincaAlkaloids: Mechanism of Action

A
  • Bind to β-tubulin and inhibit microtubule assembly

* Cell cycle specific mitosis inhibition (M-phase)

104
Q

Taxanes: Mechanism of Action

A
  • Bind to β-tubulin and stabilizemicrotubule assembly

* Cell cycle specific mitosis inhibition (M-phase)

105
Q

Taxanes

•Prototypes

A

paclitaxeland docetaxel

106
Q

paclitaxel ae

A

Hypersensitivity reactions in hands and toes, change in taste

107
Q

docetaxel ae

A
  • Greater cellular uptake; retained intracellularlylonger than paclitaxel permitting smaller dose, which reduces AEs
  • Hypersensitivity, neutropenia, alopecia
108
Q

taxanes indication

A

treatment of several solid tumors

109
Q

Type I Topoisomerases cut

A

one strand of double-stranded DNA, relax the strand, and reannealthe strand
•Inhibitors: Camptothecins(topotecan, irinotecan)

110
Q

Type II Topoisomerases cut

A

both strands of double-stranded DNA simultaneously to wind and unwind DNA supercoils
•Inhibitors:
•Epipodophyllotoxins(etoposide, teniposide)
•Anthracyclineantibiotics (doxorubicin, daunorubicin)

111
Q

Topoisomerase Inhibitors

Cell cycle specific

A

primarily S phase, also G1and G2) –except anthracyclines, which are CCNA

112
Q

Four major antineoplastic antibiotics

A
  1. Anthracyclines(doxorubicinand others)
  2. Bleomycin
  3. Dactinomycin
  4. Mitomycin
113
Q

antitumor antibiotics overview

A
  • Effects are mainly on DNA

* All of the anticancer antibiotics currently in use are products of various species of the bacterial genus Streptomyces

114
Q

Anthracyclines

drugs

A

rototype: doxorubicin

115
Q

anthracyclines moa

A
  • Inhibit topoisomerase II
  • Intercalate DNA
  • Oxygen free radicals bind to DNA causing single-and double-strand DNA breaks
  • Cell cycle nonspecific (but cycling cells are most susceptible)
116
Q

anthracyclines ae

A
  • Free radicals are linked to significant cardiotoxicity

* Cumulative cardiac damage can lead to arrhythmias and heart failure

117
Q

Bleomycin

A
  • MOA: Free radicals cause single-and double-strand DNA breaks
  • Cell cycle specific (G2arrest)
  • Causes minimal myelosuppression–useful in combination
  • Can cause significant pulmonary toxicity (5-10%, usually presents as pneumonitis with cough, dyspnea, dry inspiratory crackles)
118
Q

Dactinomycin

A
  • MOA: Intercalates DNA

* Cell cycle nonspecific

119
Q

Mitomycin

A
  • MOAs: Intercalates DNA; forms free radicals

* Cell cycle nonspecific

120
Q

Antineoplastic Enzymes

Prototypes

A

L-aspariginaseand pegaspargase(PEGylatedaspariginase

121
Q

Antineoplastic Enzymes

moa

A

hydrolyzes circulating L-asparagine into aspartic acid and ammonia, effectively inhibiting protein synthesis
•Cell cycle specific (G1)

122
Q

Antineoplastic Enzymes

ae

A
  • Acute hypersensitivity reaction
  • Delayed toxicities include an increased risk of clotting and bleeding, pancreatitis, and CNS toxicity including lethargy, confusion, hallucinations, and coma
123
Q

Antineoplastic Enzymes

indication

A

Targeted therapy for acute lymphoblastic leukemia (ALL)

•ALL tumor cells lack the enzyme asparagine synthetaseand thus require an exogenous source of L-asparagine

124
Q

The BCR-ABL fusion protein

A

results from the t(9:22) translocation and is found in 95% of patients with CML

125
Q

Imatinibis a small molecule

A

inhibitor of the ABL tyrosine kinase and has been hailed as a conceptual breakthrough in targeted chemotherapy

126
Q

Imatinibcan also inhibit

A

the RTKs PDGFR and c-KIT

127
Q

Tyrosine Kinases and Cancer

A
  • When mutated, overexpressed, or structurally altered, tyrosine kinases can become potent oncoproteins
  • Abnormal activation of tyrosine kinases has been found in many human neoplasms
  • Aberrant tyrosine kinase activity can occur in receptor tyrosine kinases or cytoplasmic kinases
  • Attractive targets for cancer therapy
128
Q

INTRACELLULAR

A

NIBS

129
Q

extracellular

A

mabs

130
Q

Erlotiniband Gefitinib

A
  • MOA: Inhibit Epidermal Growth Factor Receptor (EGFR), a receptor tyrosine kinase
  • Preferred single-agent first-line therapy for NSCLC patients with somatic activating EGFR mutations
  • Produce dermatologic toxicities
131
Q

Inhibtionof HER2/neu

A
  • The epidermal growth factor receptor HER2/neuis expressed on the cell surface of 25-30% breast cancers
  • Activation of HER2/neuinduces differentiation, growth, and proliferation
  • Trastuzumaband lapatinib
132
Q

trastuxumab and ae

A

cv complication

133
Q

cv complications withiatpatinib

A

less frequent

134
Q

alemtuzumab (not red)

Antigen
Cancer
Antigen function

A

CD52
Chronic lymphocytic leukemia
Unknown

135
Q

bevacizumab

Antigen
Cancer
Antigen function

A

VEGF
Colorectal, lung
Angiogenesis

136
Q

cetuximab
panitumumab

Antigen
Cancer
Antigen function

A

EGFR (ErbB-1)
Colorectal, lung, pancreatic, breast
Tyrosine kinase

137
Q

rituximab
ibritumomab
tositumomab

Antigen
Cancer
Antigen function

A

CD20
Non-Hodgkin’s lymphoma
Proliferation
Differentiation

138
Q

gemtuzumab (no red)

Antigen
Cancer
Antigen function

A

CD33
Acute myeloid leukemia
Unknown

139
Q

trastuzumab

Antigen
Cancer
Antigen function

A

HER2/neu
Breast
Tyrosine kinase

140
Q

The t(15;17) translocation creates

Differentiating agents…

A

the fusion protein PML-RARα, which inhibits granulocytic maturation in APL

141
Q

Tretinoin

differentitating agents

A

Tretinoin(all-trans-retinoic acid, ATRA) binds to the PML-RARαfusion protein and antagonizes the inhibitory effect on the transcription of target genes

142
Q

differentiating agents overview

A
  • Within 1-2 days the neoplastic promyelocytesbegin to differentiate into neutrophils, which rapidly die
  • One of the most successful uses of targeted therapy in cancer
  • Vitamin A toxicity and retinoic acid syndrome are common adverse effects
143
Q

Biological Response Modifiers

A

•Agents that stimulate or suppress the immune system to help the body fight cancer

Interferons
interluekin2

144
Q

interferons

moa

A

•MOA: Inhibit cellular growth, alter the state of cellular differentiation, interfere with oncogene expression, alter cell surface antigen expression, increase phagocytic activity of macrophages, and augment cytotoxicity of lymphocytes for target cells

145
Q

interleukin2

A
  • MOA: Increases cytotoxic killing by T cells and NK cells

* Major toxicity is capillary leak syndrome

146
Q

interferons ae

A

•Adverse effects: bone marrow depression, neutropenia, anemia, renal toxicity, edema, arrhythmias, and flu-like symptoms

147
Q

draw chemoman

A

now

148
Q

mucositis

A

•Methotrexate, melphalan

149
Q

peripherneuropathy

A

•Vincristine

150
Q

pulmonary fibrosis

A

•Bleomycin, busulfan

151
Q

otoxicity

A

•Cisplatin

152
Q

nephrotoxicity

A

•Cisplatin, cyclophosphamide

153
Q

hemorrhagic cystitis

A

•Cyclophosphamide, ifosfamide

154
Q

cardiotoxicity

A
  • Doxorubicin, daunorubicin

* Trastuzumab

Heme Path Exam 1 (7 decks)

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