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HemOnc Week 4 > ICL 12.1: Overview of Systemic Chemotherapies > Flashcards

ICL 12.1: Overview of Systemic Chemotherapies Flashcards

1
Q

what is precision medicine?

A

take a tumor and figure out what’s molecularly wrong with the tumor

then you design the drug to interfere with the molecular defects

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2
Q

what is personalized medicine?

A

you take an individuals cancer and design drugs that will work for that person

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3
Q

what is systemic therapy?

A

any therapy that is delivered to the total body compartment by the blood stream

they don’t effect the CNS because systemic therapies can’t cross the blood-brain barrier…

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4
Q

what type of treatments are classified as systemic therapies?

A

chemotherapies

molecular targeted agents

antibodies

hormone-targeted agents

immunotherapies

vaccines

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5
Q

which drugs are antimetabolites?

A
  1. antifolates/folic acid analogs
  2. fluoropyrimidines
  3. cytarabine
  4. gemcitabine
  5. azacytidine
  6. decitabine
  7. thiopurines
  8. purine analogs
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6
Q

which drugs are antifolates?

A

antifolates are a type of antimetabolite

aka folic acid analogs

  1. methotrexate
  2. pemetrexed
  3. pralatrexate
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7
Q

which drugs are fluoropyrimidines?

A

fluoropyrimidines are a type of antimetabolite

  1. 5-FU
  2. capecitabine
  3. TAS-102
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8
Q

which drugs are thiopurines?

A

thiopurines are a type of antimetabolite

  1. 6-mercaptopurine
  2. 6-thioguanine
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9
Q

which drugs are purine analogs?

A

purine analogs are a type of antimetabolite

  1. fludarabine*
  2. cladribine
  3. clofarabine
  4. nelarabine
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10
Q

what are gemcitabine, azacytidine, decitabine?

A

nucleoside analogs

base + sugar

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11
Q

what’s are two important property of anti-metabolites?

A

must be metabolized to their active form

they act in the S phase of the cell cycle!!

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12
Q

what are anti-metabolites?

A

designed to block DNA synthesis

antimetabolites are supposed to act better on rapidly dividing cells which is based on the idea that cancer cells divide more rapidly and go through S phase more often than normal cells so more vulnerable

originally considered to be cytostatic rather than cytotoxic but now it’s recognized that many produce cell death by triggering apoptosis

most are nucleoside analogues that interfere with DNA synthesis or block methylation of uracil to thymidylate

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13
Q

which types of cells are more vulnerable to antimetabolites?

A

GI and skin

because they have high turnover

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14
Q

what do antimetabolites do?

A

compete, replace or inhibit a specific metabolite of a cell and thereby interferes with the cell’s normal metabolic functioning

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15
Q

what are the three sub-classes of antimetabolites?

A
  1. folic acid analogs = inhibit folate dependent reactions in the cell
  2. pyrimidine analogs
  3. purine analogs and related inhibitors
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16
Q

which drugs are folic acid analogs?

A
  1. methotrexate
  2. pemetrexed
  3. pralatrexate
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17
Q

which drugs are pyrimidine analogs?

A
  1. fluorouracil
  2. cytarabine
  3. gemcitabine
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18
Q

which drugs are purine analogs?

A
  1. mercaptopurine

2. pentostatin

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19
Q

which disease is pentostatin used to treat?

A

hairy cell leukemia

pentostatin is a purine analog

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20
Q

what is folate?

A

an essential dietary factor from which THF cofactors are formed which provide single carbon groups for the synthesis of precursors of DNA and RNA

THF is a one-carbon donor

to function as a cofactor, folate must be reduced by DHFR to THF

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21
Q

what enzyme do antifolate drugs target?

A
  1. DHFR
  2. THF

DHFR reduces folate to THF

THF is a one-carbon donor for DNA precursors

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22
Q

what does methotrexate do?

A

inhibits dihydrofolate reductase (DHFR)

DHFR reduces DHF to THF

THF is then used in the reaction:
dUMP –> dTMP via thymidylate synthase

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23
Q

what does 5-FU do?

A

inhibits thymidylate synthase so it also has an effect on dividing cells and inhibiting DNA synthesis

normally, dUMP –> dTMP via TS

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24
Q

what’s a potential problem with giving someone 5-FU?

A

DPD normally breaks down 5-FU

some people lack DPD enzyme and can have really toxic side effects if you give them 5-FU so you just have to watch out

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25
Q

what is the mechanism of action of antifolate drugs?

A

they inhibit DHFR which results in the depletion of reduced folate (THF)

no THF inhibits de novo purine and pyrimidine biosynthesis and hence, DNA synthesis

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26
Q

which phase of the cell cycle do antifolates effect?

A

they exert their effects in the S-phase of the cell cycle by inhibiting DNA synthesis

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27
Q

how are antifolates transported into the cell?

A

by specific transport proteins RFC & FRP

RFC = reduced folate carrier

FPGS = folylpolyglutamate synthase

then they’re metabolized by FPGS to polyglutamated forms to exert cytotoxic effects

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28
Q

how does methotrexate enter the cell?

A

MTX is an analogue of dihydrofolic acid (DHF)

enters the cell through RFC1 = reduced folate carrier 1

once inside the cell, MTX (also known as MTXGlu1 because it’s a monoglutamate) is converted into its active polyglutamated forms (MTXGlu2-5) by the enzyme FPGS

the sequential addition of up to four glutamate residues prevents efflux of MTX from the cell

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29
Q

what does MTX do?

A

inhibits DHFR, TS and some other early steps in purine biosynthesis

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30
Q

what’s the principal site of action for pemetrexed?

A

inhibition of TS and purine biosynthesis

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31
Q

what does DHFR do?

A

H2-folate –> N5, N10, methylene H4-folate

simplified version:
DHF –> THF

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32
Q

what does TS do?

A

dUMP –> dTMP

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33
Q

what are some of the clinically toxic side effects of MTX?

A
  1. myelosuppressive = drops the blood counts and increases risk for infection
  2. causes mucositis because all the GI mucosa are rapidly growing so they’re very effected by MTX
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34
Q

how is MTX cleared?

A

it’s cleared by the kidneys

so you have to reduce its dose if someone is in kidney failure

MTXGlu2-5 are retained in hepatic and renal tissues for long periods of time causing prolonged suppression of THF in these cells

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35
Q

what is the MTX rescue drug?

A

leucovorin

if you give too much MTX, give leucovorin

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36
Q

what does leucovorin do?

A

MTX rescue drug

it’s a form of THF that can be readily taken up by cells

if it is administered after overdosing with MTX it can supply THF needed for cell survival until the MTX polyglutamate is finally broken down to free MTX and leaves the cell by diffusion

with high-dose MTX and leucovorin rescue, the patient must be well-hydrated and urine alkalinized, or MTX will precipitate in acidic tubular fluid

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37
Q

what do pyrimidine and purine analogs do?

A

either inhibit nucleotide synthesis or get incorporated into the DNA blocking its function

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38
Q

which bases are purines?

A

adenosine

guanine

*2 rings

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39
Q

which bases are pyrimidines?

A

thymidine

cytosine

uracil

*1 ring

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40
Q

capecitabine is an analog to which base?

A

cytosine

so it’s a pyrimidine analog

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41
Q

6-merceptopurine is an analog to which base?

A

guanine

so it’s a purine analog

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42
Q

5-FU is an analog to which base?

A

thymines

so it’s a pyrimidine analog

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43
Q

cladribine is an analog to which base?

A

adenine

so it’s a purine analog

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44
Q

fludarabine is an analog to which base?

A

adenine

so it’s a purine analog

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45
Q

what disease is fludarabine often used to treat?

A

chronic lymphocytic anemia

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46
Q

which drugs are pyrimidine analogs?

A
  1. capecitabine

2. 5-FU

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47
Q

which drugs are purine analogs?

A
  1. 6-mercaptopurine
  2. 6-thioguanine
  3. fludarabine
  4. cladribine
  5. pentostatin
  6. azathioprine
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48
Q

what are the side effects of 5-FU?

A
  • myelosuppression if given via bolus
  • alopecia
  • dermatitis
    nausea/vomiting

depends on how you give the drug

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49
Q

what are the side effects of capecitabine?

A
  • myelosuppression
  • alopecia
  • dermatitis
    nausea/vomiting

** increased incidence of hand and foot syndrome if you give it via IV/constant fusion

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50
Q

what is hand and foot syndrome?

A
  • tingling, burning, or numbness
  • redness or swelling
  • flaking or peeling skin
  • small blisters
  • sores or breaks in the skin
  • discomfort or pain
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51
Q

what’s the relationship between capecitabine and 5-FU?

A

they’re both pyrimidine analogs - capecitabine gets converted into 5-FU

capecitabine has to first get changed in the liver and then it gets changed again in the cell

in the cell is where it gets made into 5-FU

52
Q

what happens if you’re giving warfarin or cumadin with capecitabine?

A

capecitabine is being metabolized in the liver, it’s competing with the enzymes in the liver

warfarin will increase PT so it’s a drug-drug interaction

53
Q

what’s the effect of grape juice fruit on p450 system of metabolizing drugs?

A

it’s an inducer of the enzymes

it can effect the metabolism of drugs and increase the toxicity of drugs in the liver

a lot of times, patients want to know about alternative medicine but in this case grapefruit juice can be harmful

54
Q

what is another name for cytarabine?

A

cytosine arabinoside = Ara-C

it’s an antimetabolite that is a **nucleoside! aka it’s a base +sugar

55
Q

what disease is Ara-C used to treat?

A

it’s an antimetabolite used in the therapy of AML

AML has a super high doubling time and Ara-C is an antimetabolite so it has a strong effect on rapidly dividing drugs!

56
Q

how does Ara-C enter the cell?

A

by using the nucleoside transporter hENT1

57
Q

how does Ara-C work?

A

it competes with the physiological substrate deoxycytidine 5′- triphosphate (dCTP) for incorporation into DNA by DNA polymerases

incorporated Ara-CMP residue is a potent inhibitor of DNA polymerase, both in replication and repair synthesis, and blocks the further elongation of the nascent DNA molecule

58
Q

how do you give Ara-C

A

continuous infusion

7 days of continuous infusion in combination with anthracycline

must be continuous infusion because 85% of the drug is deaminated by 2 deaminases in the blood stream so it’s rapidly degraded

59
Q

what are the side effects of Ara-C?

A

wipes your bone marrow out…

it’s a potent myelosuppressive agent capable of producing acute, severe leukopenia, thrombocytopenia, and anemia with striking megaloblastic changes

but this is kinda what you want when you’re treating AML

60
Q

is cytarabine cell cycle dependent?

A

yes!

it’s an antimetabolite so it effects S phase

61
Q

what is azathioprine used for?

A

it’s a purine analog

rarely used to treat cancer, it is mostly used as an immunosuppressant

is a pro-drug, converted in the body to the active metabolite 6- mercaptopurine

62
Q

what is the MOA of azathioprine?

A

it’s a purine analog that’s a pro-drug, converted in the body to the active metabolite 6- mercaptopurine

drug metabolism results in the incorporation of thiopurine analogues into the DNA structure, causing chain termination and cytotoxicity

63
Q

what happens to azathioprine in the body?

A

azathioprine –> 6-MP –> 6-thioinosinic acid –> 6-thioguanine nucleotides

6-thioinosinic acid inhibits purine synthesis

6-thioguanine nucleotides get incorporated into RNA and DNA

64
Q

what does TPMT enzyme do?

A

6-MP –> 6-CH3MP

TPMT = thiopurine methyl transferase

5% of the population have decreased/missing amount of TPMT

so without it, if you’re giving someone purine analogs like azathioprine, you cam get super toxic levels of the purine analogs

65
Q

what does XO stand for?

A

xanthine oxidase

involved in purine synthesis, specifically production of uric acid

66
Q

is gout a disorder of purine or pyrimidine synthesis?

A

purine synthesis

XO enzyme is involved in the production of uric acid

67
Q

what foods do you tell gout patients to avoid?

A

meat

beer

these foods are high in uric acid

68
Q

what is gout?

A

uric acid crystals in the joints - usually the toe

it’s form of arthritis characterized by severe pain, redness, and
tenderness in joints

pain and inflammation occur when too much uric acid crystallizes and deposits in the joints

69
Q

how do you diagnose gout?

A

you aspirate and look for uric acid crystals under the microscope

70
Q

what does XO do and which condition is it responsible for?

A

XO catalyzes 6-MP to 6-thiouric acid (inactive)

so ultimately it’s responsible for formation of urate from purines which leads to gout!

71
Q

which drug is used to treat gout? what does it do?

A

allopurinol

allopurinol inhibits XO which normally catalyzes 6-MP to 6-thiouric acid

72
Q

will a pharmacist warn you of a drug-drug interaction if you order a purine analog drug for a patient who is already taking allopurinol?

A

if someone is on allopurinol and you want to treat them with a purine analog, you’re going to have to reduce the dose of purine analog to avoid drug toxicity

a purine analog, like azathioprine for example, is going to generate a lot of 6-MP

without XO, 6-MP will buildup and cause toxicity

73
Q

what’s a side effect of azathioprine?

A

uric acid buildup

so sometimes when you start to treat cancer with azathioprine which is a purine analog, you can get uric acid buildup

a lot of times then you have to use allopurinol to prevent uric acid buildup

74
Q

how do alkylating agents work?

A

they cross link DNA and cause damage

they’re super reactive and really nasty

they’re all immunosuppresing!!

75
Q

what are the sub-classes of alkylating agent drugs?

A
  1. nitrogen mustards
  2. nitrosoureas
  3. alkyl sulphonates
  4. atypical
76
Q

which drugs are nitrogen mustard alkylating agents?

A
  1. mecholrethamine
  2. cyclophosphamide
  3. ifosfamide
  4. melphalan
  5. chlorambucil
77
Q

which drugs are nitrosoureas alkylating agents?

A
  1. carmustine (BCNU)
  2. steptozocin
  3. bendamustine
78
Q

which drug is an alkyl sulphonate alkylating agent?

A

busulphan

79
Q

which drugs are atypical alkylating agents?

A
  1. procarbazine
  2. dacarbazine
  3. temozolomide

THESE DRUGS CROSS THE BLOOD BRAIN BARRIER!!!

80
Q

what is temozolamide used to treat?

A

to treat gliomas, brain cancers

often used in combination with radiation

***it crosses the blood brain barrier!!!!!

81
Q

are alkylating agents cell cycle dependent?

A

no

they are cell-cycle non-specific drugs

82
Q

what is the MOA of alkylating agents?

A

they’re highly reactive compounds that cross link DNA, RNA and proteins by binding to electron rich areas, specifically, guanine in DNA

alkylating agents form highly reactive carbonium ion intermediates which covalently link to sites of high electron density, such as phosphates, amines, sulfhydryl, and hydroxyl groups

their chemotherapeutic and cytotoxic effects are directly related to the alkylation of reactive
amines, oxygens, or phosphates on DNA

83
Q

which types of drugs are cell cycle non-specific drugs?

A
  1. alkylating drugs
  2. nitrosoureas
  3. cisplatin
  4. procarbazine
  5. antitumor antibiotics
  6. dacarbazine
84
Q

what is the most commonly used alkylating agent?

A

cyclophosphamide

doesn’t have a super high therapeutic index

it has to be activated by the hepatic CYP2B enzymes

in order to get an active byproduct, the liver has to metabolize it to its active byproduct

85
Q

what is a therapeutic index?

A

has to do with how much bang you get your buck

if you have a precision drug, it has a super high therapeutic index

86
Q

what are the side effects of alkylating agents?

A
  1. neurotoxicity: nausea, vomiting common after nitrogen mustard or BCNU
  2. myelosuppressive!! since BM is rapidly producing, they suppress BM which also leads to immune suppression
  3. mucosal toxicity: alkylating agents are highly toxic to dividing mucosal cells and to hair follicles, leading to oral mucosal ulceration, intestinal denudation, and alopecia
87
Q

which alkylating agent is the most neurotoxic?

A

ifosfamide

the most neurotoxic agent of this class and may produce altered mental status, coma, generalized seizures, and cerebellar ataxia

88
Q

what diseases can alkylating agents lead to?

A

busulphan & cyclophosphamide can cause pulmonary fibrosis and veno-occlusive disease

this will also lead to SIADH

alkylating agents can also lead to male/female reproductive damage

89
Q

what are the platinum coordinating complexes?

A
  1. cisplatin
  2. carboplatin
  3. oxaliplatin
90
Q

what is the MOA for platinum drugs?

A

they’re part of the alkylating agents superfamily

they bind to nucleophilic sites on DNA and cause DNA damage (both intra and interstrand covalent links)

inside the cell, chloride is replaced by water and the drug is activated. High concentrations of chloride stabilize the drug reducing its cytotoxicity

91
Q

are platinum coordination complexes cell specific?

A

no

92
Q

what are the side effects of cisplatin?

A

nephrotoxicity and ototoxicity

CNS toxicity is more severe than other AA

marked nausea and vomiting, peripheral neuropathy

myelosuppression

93
Q

what cancers is cisplatin useful for treating?

A

very useful for a variety of solid tumors:

testicular, ovarian, head and neck, and lung cancers

94
Q

what’s the difference between cisplatin and carboplatin?

A

cisplatin is very kidney toxic

when you get cisplatin you have to pre and post hydrate

but carboplatin is much more myelosuppressive

95
Q

which drugs are vinca alkaloids?

A
  1. Vincristine (most common, most myelosuppressive)
  2. Vinblastine
  3. Vinorelbine
96
Q

what do vinca alkaloids do?

A

inhibition of tubulin polymerization, which disrupts assembly of microtubules, an important part of the mitotic spindle

they bind to β-tubulin and prevent its interaction with ɑ-tubulin

they arrest the cell in metaphase which stops cell division and leads to cell death

97
Q

are vinca alkaloids cell cycle specific?

A

yes

they arrest the cell in metaphase which stops cell division and leads to cell death

98
Q

vinca alkaloids are active in which phase of the cell cycle?

A

M phase

99
Q

what is vinblastine most used for?

A

testicular cancer and HL

vinblastine is myelosuppressive!

vinBlastine = Bone marrow suppression

100
Q

what is vincristine most used for?

A

vincristine with prednisone is very useful for childhood leukemias

vincristine is neurotoxic!

viNcristine = Neurotoxic

101
Q

which drugs are taxanes?

A
  1. paclitaxel

2. docetaxel

102
Q

what are taxanes?

A

hyper-stabilizes microtubule structure = freezes them

they bind to the β subunit of tubulin ,the resulting microtubule/taxane complex does not have the ability to disassemble

this adversely affects cell function because the shortening and lengthening of microtubules is necessary for their function

this results in apoptosis of cancer cells

103
Q

what phase of the cell cycle do taxanes effect?

A

M phase

microtubules

104
Q

when do you have to watch out for the dose of taxanes?

A

if there’s hepatic dysfunction

105
Q

what are taxanes used to treat?

A

they have become central components of regimens for treating metastatic ovarian, breast, lung, GI, genitourinary, and head and neck cancers

106
Q

what are the side effects of taxanes?

A

myelosuppression

neuropathy!! neurons rely on microtubules

107
Q

what are topoisomerase?

A

DNA topoisomerases are nuclear enzymes that reduce torsional stress in supercoiled DNA

this allows for selected regions of DNA to become sufficiently untangled and relaxed to permit replication, repair, and transcription

type I: cuts one strand

type II: cuts two strands

108
Q

what phase of the cell cycle do topoisomerase I inhibitors effect?

A

S phase

***topoisomerase II are NOT cell cycle dependent

109
Q

which drugs are topoisomerase i inhibitors?

A

irinotecan

topotecan

110
Q

what do topoisomerase I inhibitors do?

A

the initial cleavage action of topoisomerase I is not affected but the re-ligation step is inhibited

this leads to the accumulation of single-stranded breaks in DNA

the collision of a DNA replication fork with this cleaved strand of DNA causes an irreversible double-strand DNA break, ultimately leading to cell death

111
Q

what are some side effects of topoisomerase I inhibitors?

A

myelosuppression

diarrhea

112
Q

what are anthracyclines?

A

they inhibit topoisomerase II

they to DNA through intercalation, with consequent blockade of the synthesis of DNA and RNA, and DNA strand scission

they are NOT cycle dependent!!

113
Q

which drugs are anthracyclines?

A
  1. doxorubicin
  2. daunorubicin
  3. mitoxantrone
114
Q

are anthracyclines cell cycle dependent?

A

no!

they act at multiple phases during the cell cycle

115
Q

what is doxorubicin?

A

anthracycline/topoisomerase II inhibitor

anticancer drug with major clinical activity in several cancers

116
Q

what’s the major side effect with doxorubicin?

A

cardiotoxicity!!

creates ROS that damage the heart

acute: arrhythmias
chronic: digitalis-resistant congestive heart failure; lifetime dose dependent - 20% of patients receiving 550 mg/m2

117
Q

what is etoposide?

A

inhibitor of topoisomerase II

118
Q

what is etoposide used to treat?

A

primarily used for treatment of testicular tumors, in combination with bleomycin and cisplatin, and in combination with cisplatin and ifosfamide for small cell carcinoma of the lung

119
Q

what are the side effects of etoposide?

A

it’s leukemogenic and may cause acute nonlymphocytic leukemia in children

myelosuppression

120
Q

what is bleomycin?

A

DNA cleaving antibiotic

water soluble, basic glycopeptide with a core of either Fe2+ or Cu2+

it’s metabolized by hydrolases found in almost all tissues except, skin and lungs

121
Q

what are the side effects of bleomycin?

A

cytotoxicity results from its ability to cause oxidative damage to the deoxyribose of thymidylate and other nucleotides, leading to single- and double-stranded breaks in DNA

damaged cells accumulate in the G2 phase of the cell cycle

**toxicity to skin and lungs

122
Q

what is bleomycin used to treat?

A

highly effective against germ cell testicular cancer and HL

123
Q

is bleomycin cell cycle specific?

A

yes

G2 and M phases

124
Q

what is the skin toxicity side effects seen in bleomycin?

A

hyperpigmentation, hyperkeratosis, erythema, and even ulceration

rarely, patients with severe skin toxicity may experience Raynaud’s phenomenon

125
Q

which groups of drugs cause neuropathy?

A

taxanes and vinca alkaloids

anything effecting the microtubules because neurons rely on microtubules

HemOnc Week 4 (10 decks)

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