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HDT 3.2 > Cancer Treatment > Flashcards

Cancer Treatment Flashcards

1
Q

what are some drugs of alkylating agents and nitrosureas?

A

ifosfamide, cyclophosphamide, melphalan, chlorambucil, cisplatin, carmustine

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2
Q

what is the MOA of alkylating agents and nitrosureas?

A

addition of an alkyl group to nucleic acids/proteins/DNA
= inhibition of DNA replication = increase mutations (=secondary cancer) or cell death
any time of cell cycle

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3
Q

what are the main side effects of alkylating agents and nitrosureas?

A

teratogenic and carcinogenic

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4
Q

name sub classes of alkylating agents

A

a) Nitrogen mustards
b) Alkyl sulfonates (e.g. busulfan)
c) Triazines (e.g. dacarbazine, temozolomide)
d) Nitrosoureas (e.g. carmustine, lomustine)
e) Metal salts

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5
Q

what is mechlorethamine?

A

also known as Mustine

rarely used
short half life
very corrosive = toxic
tissue damage
nausea and vomiting side effects

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6
Q

what is melphalan?

A

oral given for myeloma - cancer of plasma cells
IV conditioning pre-transplant

increased risk of myelodysplasia with prolonged use

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7
Q

what is Cyclophosphamide?

A

A type of chemotherapy
activated in the liver, and broken down into into acrolein and etc.

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8
Q

what is acrolein?

A

bladder irritant
risk of haemarradic cystitis

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9
Q

what is the antidote for acrolein? and how?

A

MESNA
mops up the acrolein

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10
Q

what is bendamustine?

A

licenced for CLL and NHL

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11
Q

what are metal salts?

A

cisplatin, carboplatin and oxaliplatin

inhibit DNA synthesis via inter/intra- strand cross links mainly binding to GUANINE

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12
Q

whats cisplatin’s half life?

A

long half life
60 hours

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13
Q

what are side effects of metal salts?

A

nephrotoxic
neurotoxic - nause/vomiting

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14
Q

what are antimetabolites?

A

exert cytotoxic effects to natural metabolites involved in nucleic acid synthesis

The cell mistakes them for a normal metabolites, resulting in:
- inhibition of critical enzymes involved in nucleic acid
synthesis
- incorporation into the nucleic acid, leading to incorrect codes

LARGELY S-PHASE SPECIFIC

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15
Q

examples of anti-metabolites?

A

folate antagonists
pyrimidine analogues
purine analogues
ribonucleotide reductase inhibitors

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16
Q

MOA of 5-FU drugs

A

is a pyrimidine analogue that can be misincorporated into RNA and DNA in place of uracil or thymine

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17
Q

what is DHFR?

A

reduction enzyme

dihydrofolate reductase responsible for folates to be reduced to tetrahydrofolate -responsible for thymidine and purine synthesis

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18
Q

what is folate antagonists?

A

competitively inhibit DHFR= inhibit thymidine and purine synthesis

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19
Q

name some examples of folate antagonsists?

A

MTX
pemetrexed
raltitrexed

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20
Q

what is MTX?

A

inhibit dihydrofolate reductase (DHFR), leading to inhibition of DNA and RNA synthesis.

renally cleared- largely unchanged
half life- 8-10hrs may accumulate to 24-36hrs

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21
Q

when is folic acid prescribed w MTX?

A

alternate days to MTX dose
one per day or once a week

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22
Q

why can folic acid not be co-prescibed with MTX?

A

MTX 100,000x affinity for enzyme than folic acid

Folic acid may interfere with the gastrointestinal absorption of methotrexate.

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23
Q

what can large amounts of DHFR cause?

A

mtx resistance

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24
Q

how can mtx resistance be overcome

A

increase mtx dose

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25
Q

why is folic acid prescribed w mtx?

A

for treatment/rescue to healthy cells = reduce toxicity to healthy cells = decrease side effects

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26
Q

mtx side effects

A

myelosuppresion
mucositis
renal toxicity
alkalisation of urine and vigorous hydration alongside mtx administration

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27
Q

why do we monitor urine pH w MTX?

A

acidity of urine due to MTX crystallisation which can cause kidney damage
to alkalise using sodium bicarb

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28
Q

mtx drug interactions

A

aspirin/ciprofloxacin/NSAIDs = reduce tubular secretion of MTX due to renal tubular competition = increase toxicity

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29
Q

what is leucovorin/folinic acid?

A

form of THF
maintain normal cell functions - reverses MTX toxicity

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30
Q

when will leucovorin/folinic acid be given?

A

mucositis and myelsuppression

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31
Q

what is mucositis?

A

when your mouth or gut is sore and inflamed

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31
Q

what is pyrimidine analogues?

A

fraudulent nucleotides - cytosine, thymine and uracil

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32
Q

examples of pyrimidine analogues?

A

5-fluorouracil (5-FU),
gemcitabine,
capecitabine - erratic oral absorption

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33
Q

what is 5-FU?

A

a pyrimidine analogue
activated to 5-F-dUMP= inhibits thymidylate synthase =
inhibits RNA SYNTHESIS

15mins half life - therefore prolonged infusions/bolus needed
eratic oral absorption

colorectal/breast/stomach/oesophagus/head/neck carcinomas

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34
Q

how can we stabilise 5-F-dUMP?

A

co-administer folinic acid = enhances activity

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35
Q

what is capecitabine?

A

oral 5-FU drug
prodrug
conversions to 5-FU within the liver and tumour cells

breast/gastric/pancreatic cancer

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36
Q

is capecitabine or 5-FU better?

A

capecitabine better tolerated more
but experience more hand and foot syndrome

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37
Q

what is Gemcitabine?

A

Converted to gemcitabine triphosphate which is incorporated into DNA in place of deoxycytidine triphosphate.

  • Given weekly.
  • Licensed for pancreatic cancer, non-small cell lung cancer, bladder
    cancer and breast cancer.
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38
Q

what is Cytarabine?

A

Converted to active form, ara-CTP which inhibits DNA polymerase.

  • May also be directly incorporated into DNA chain, preventing replication and making it more susceptible to degradation.
  • Most useful in tumours with high growth fraction, and mainly used for AML, ALL and certain lymphomas.
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39
Q

what is purine analogues?

A

Can be incorporated into the growing DNA chain in place of the natural nucleotides adenine & guanine
* Can also inhibit the enzymes involved
* May kill cells, including cancer cells

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40
Q

give examples of purine analogues?

A

6-mercaptopurine, 6-thioguanine, fludarabine

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41
Q

what is 6-mercaptopurine?

A

prodrug - oral
inhibits various metabolic reactions including purine biosynthesis

azathioprine

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42
Q

what is fludarabine?

A

The active triphosphate, 2F-ara-ATP inhibits a variety of enzymes involved in DNA synthesis
ORAL

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43
Q

what is an example of rinbonucleotide reductase inhibitor?

A

hydroxycarbamide

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44
Q

what is the MOA of hydroxycarbamide?

A

Inhibitor of ribonucleotide reductase, an enzyme essential for the generation of deoxyribonucleotides
* Prevents purines and pyrimidines synthesis= decrease DNA conc.
* May also damage DNA = inhibit DNA repair.
* Used in haematological malignancies – CML, polycythaemia,
thrombocythaemia
* Given orally as 500mg capsules – dose tailored to response

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45
Q

what are the antimetabolites MOA?

A
  1. folate antagonists
    - inhibit the action of folates which are co-factors essential for nucleotide synthesis
  2. pyrimidine analogues
    - mimic/inhibit synthesis of cytosine, thymine & uracil thereby
    interfering with DNA synthesis
  3. purine analogues
    - mimic/inhibit synthesis of adenine & guanine interfering with DNA synthesis
  4. ribonucleotide reductase inhibitors
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46
Q

what are the classes of mitotic inhibitors?

A

vinca alkaloids -vincristine
taxanes

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47
Q

moa of mitotic inhibitors

A

act on microtubules in the nucleus = arresting metaphase = inhibit mitosis

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48
Q

what are examples of vinca alkaloids?

A

vincristine, vinblastine,
vindesine, vinorelbine

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49
Q

what is the MOA of vinca alkaloids?

A

bind to tubulin = prevent microtubule assembly

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50
Q

what is vincristine?

A

used in haematology,
indication - sarcoma and neuroblastoma

can cause neurotoxicity n mild myelosuppression
metabolised in the liver and excreted in faeces via cyto P450

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51
Q

what are examples of taxanes?

A

paclitaxel
docetaxel
abraxane
cabazitaxel

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52
Q

explain taxanes/ paclitaxel

A

indication - ovarian /breast cancer
stabilisers of microtubule
poor water solubility
risk of hypersensitivity reactions, neutropenia , neurotoxicity, alopecia, cardiotoxicity

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53
Q

what are Topoisomerase inhibitors?

A

nuclear enzymes that cause DNA strand breaks and therefore allow it to unwind during cell division.

Inhibitors stabilise the enzyme-DNA complex and prevent re-ligation, resulting in irreversible DNA strand breaks.
S/G2 phase of the cell cycle

  • Topoisomerase I - causes single nick in DNA
  • Topoisomerase II - cleaves both strands
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54
Q

what are the types of Topoisomerase inhibitors?

A
  • Topoisomerase I - causes single nick in DNA
  • Topoisomerase II - cleaves both strands
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55
Q

what can inhibit topoisomerase II?

A

etoposide

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56
Q

indications of etoposide?

A

oral/iv

small cell lung cancer/ testicular cancer /lymphoma

57
Q

what are some example of topoisomerase I ?

A

topotecan
irinotecan

58
Q

what are some antitumour antibiotics?

A
  1. anthracyclines
    - inhibition of topoisomerase II
    - DNA intercalation
    - free radical formation
    - alkylation
  • Examples include:
  • doxorubicin, daunorubicin
  • idarubicin, epirubicin
  1. mitoxantrone
  2. actinomycin D
  3. mitomycin C
  4. bleomycin
59
Q

what is mitoxantrone?

A

Structurally related to anthracyclines
* Does not produce free radicals so less cardiotoxic
* Indications include AML, breast cancer, prostate cancer.

60
Q

what is actinomycin D?

A

Binds to DNA and inhibits DNA-dependent RNA synthesis. Also inhibits topoisomerase II.
* Used for sarcomas.

61
Q

what is mitomycin C?

A

Causes cross-links between complementary DNA strands, which inhibits replication.
Commonly used for lung cancer. Also given intravesically for bladder cancer.
Causes delayed myelosuppression.

62
Q

what is bleomycin?

A

Causes DNA strand scission - resulting in fragmentation of DNA.
Indications include testicular cancer, Hodgkin’s and NHL.
Risk of cumulative pulmonary toxicity.

63
Q

why are biologics used in cancer treatment ?

A

using understanding of biology of the tumour and TME to control the disease

e.g. allowing switching of cytokines relative to the TME

64
Q

what is rituximab like as a biologic ?

A

more targeted biologic - monoclonal antibody
targets antigens expressed on the cancer cell

65
Q

what is thalidomide like as a biologic ?

A

non specific biologic
modulates the immune system

66
Q

what is the main treatment of chronic myeloid leukaemia (CML)?

A

allogenic SCT - stem cell treatment

given with a large amount of chemo therapy

this allows the immune system to be restored

67
Q

what are the types of cytokines?

A

Interleukin-2
* Produced by activated T-cells.
* Stimulates T-cell proliferation and activates NK cells.
* Has been used in renal cell cancer and melanoma.

Interferon-alpha
* Possesses a variety of immunomodulatory effects
e.g. activation of NK cells modulation of antibody production inducing antigen presentation on tumour cells

68
Q

what is an example of an immunomodulator?

A

thalidomide

69
Q

what indication is interferon-alpha used for?

A

renal cell
carcinoma

70
Q

describe thalidomide use in cancer?

A

inhibit angiogenesis = prevent tumour spread

immunodulation too ! alters immune response

71
Q

how are monoclonal antibodies used in cancer treatment?

A

Binding to tumour-associated antigens

Destruction of the tumour cell by blocking the growth and spread of cancer cells by interfering with cellular functions necessary for their survival.

72
Q

when are checkpoint blockade used in cancer treatment?

A

used in haematology and oncology

73
Q

what are some examples of checkpoint blockades in cancer treatment?

A

Pembrolizumab and nivolumab inhibit PD-1 and have multiple indications – melanoma, lung, bladder, renal cell, head and neck , Hodgkin lymphoma

Atezolizumab is a PD-L1 inhibitor – used for bladder and lung

Ipilumumab – inhibits CTLA-4 and is used to treat advanced
melanoma

OPPOSITE
Abatacept – enhances CTLA-4 and can be used for RA, kidney transplant rejection

74
Q

describe Ipilimumab

A

antibody binds to CTLA4 on a T cell = activate T cell by blocking B7 + CTLA4 process (= inactivate T cell)

75
Q

describe nivolumab/pembrolizumab

A

blocks overexpressed PDL1 and blocks PD1 on cancer cells = T cell activation

PDL1+PD1 binding = T cell inactivation

76
Q

describe rituximab

A

A monoclonal antibody, specific for CD20, expressed on the surface of mature B cells.
* After binding Rituximab causes cell death by:
- induction of apoptosis
- activation of patient’s immune system
- sensitisation of resistant lymphoma cells to conventional chemotherapy

77
Q

what are the ways rituximab induces cell death?

A
  • induction of apoptosis
  • activation of patient’s immune system
  • sensitisation of resistant lymphoma cells to conventional chemotherapy
78
Q

what are the side effects of rituximab?

A

infusion related
e.g. fever/chills/rigors

RARE: cytokine release syndrome - can be fatal

79
Q

why do you get fevers/chills/rigors from taking rituximab?

A

due to foreign substances/antibodies inducing an immune response

80
Q

how do you prevent rituximab from getting side effects?

A

pre-medicate with antihistamine/paracetamol/steroids

or slow down the infusion rate

81
Q

describe trastuzumab/ HERCEPTIN

A

antibody against HER2 antigen which is over-expressed in some breast cancer cells

monotherapy or in combo

82
Q

what occurs between trastuzumab/ HERCEPTIN and doxorubicin?

A

concerns of cardiac toxicity

83
Q

describe alemtuzumab

A

antibody against CD-52, against specific lymphocytes

used for T cell depletion prior to allogenic BMT

used for Chronic Lymphocytic Leukaemia (CLL) and Multiple sclerosis

84
Q

describe how T cell cancer therapy to kill tumour cells

A
  1. blood drawn from the pt and T cells are separated out
  2. t cells are genetically engineered to produce surface receptors called Cars
    • Cars recognised and attaches to specific proteins on tumour cells
  3. cars T cells multiply while the pt has chemotherapy to kill off existing t cells
  4. transfer t cells into the body to recognise and kill cancerous cells
85
Q

what does Cars do?

A

produced from genetically engineered T cells
target CD19 on B cells
Cars recognised and attaches to specific proteins on tumour cells

86
Q

when are CARS used?

A

treat advanced B-ALL, advanced non-hodgkin lymphoma and mantle cell lymphoma

87
Q

whats a risk of CARS?

A

cytokine release syndrome and neurological complications

88
Q

what are the symptoms of cytokine release syndrome

A

fever, nausea, headache, rash, rapid heartbeat, low blood pressure, and trouble breathing

89
Q

what are the subtypes of targeted therapies?

A
  • proteasome inhibitors
  • protein kinase inhibitors/nibs
  • PARP inhibitors
  • BCL-2 inhibitors
  • Hedgehog pathway inhibitors
  • VEGF inhibitors
90
Q

describe proteasomes

A

key roll in cellular degradation - accumulation of proteins = toxic to cells

91
Q

what are proteasome inhibitors used to treat?

A

multiple myeloma

92
Q

what is bortezomib ?

A

a proteasome inhibitor

IV bolus inf. and SC

93
Q

describe the side effects of bortezomib

A

neuropathy
thrombocytopenia
fatigue

94
Q

describe the side effects of proteasome inhibitors

A

neuropathy
thrombocytopenia
fatigue

95
Q

name some proteaome inhibitors

A

bortezomib -iv inf/sc
carfilzomib -iv inf
ixazomib -oral

96
Q

describe protein kinase inhibitors/nibs

A

target growth factors on receptors of cancer cells

oral therapies
given continuously

97
Q

give an example of nibs

A

imatinib
FLT-3 inhibitors

98
Q

what is imatinib used for

A

CML used for BCR-ABL

BCR-ABL kinase selective inhibitor

99
Q

what are the common side effects of imatinib

A

haematological toxicities
diarrhoea
rash
oedema
nausea
cramps
headache

100
Q

what are some drug interactions of imatinib

A

itraconazole, clarithromycin, phenytoin, rifampicin, warfarin, ciclosporin

101
Q

what are FLT-3 inhibitors

A

FLT3 mutations occur im AML

inhibits mutations properties:
cellular growth
anti-apoptotic signalling
cellular survival

102
Q

what are PARPi used for?

A

ovarian and breast cancer

103
Q

what are some examples of PARPi

A

olaparib, niraparib, rucaparib - ovarian cancer

olaparib, talazoparib - breast cancer

104
Q

describe PARPi

A

inhibit PARP enzymes used for DNA repair of cancerous cells = cell death

generally require BRCA mutation to cause cell death

105
Q

describe BCL-2 inhibitors

A

inhibit BCL-2 = overexpressed in many cancers e.g. CLL

BCL-2 inhibits BAX/BID/BAK= inhibit cyto c release from mitochondria = no caspase enzymes released = no cellular apoptosis

106
Q

what is an example of BCL-2 inhibitor?

A

venetoclax

107
Q

what is venetoclax?

A

BCL-2 inhibitor

used for CLL and AML and others. - lymphoma/myeloma

108
Q

what are the side effects of venetoclax?

A

tumour lysis syndrome (TLS) so start with a low dose and titrate up

109
Q

why is a lower dose of venetoclax given in AML

A

as venetoclax is given with posaconazole = increases venetoclax conc. systemically therefore we can give a lower dose to give a similar efficacy of venetoclax

without risk of TLS

110
Q

describe VEGF inhibitors

A

inhibit VEGF = inhibit angiogenesis = prevent tumour growth and spread

VEGF = promotes angiogenesis

111
Q

what are some examples of VEGF inhibitors

A
  • MABs e.g. bevacizumab, ramucirumab
    – TKIs e.g. sunitinib, axitinib. Commonly for kidney cancer
    – Aflibercept (a modified antibody)
112
Q

when should you take etoposide capsules?

A

before food

113
Q

when should you take uftoral capsules?

A

before food

114
Q

when should you take capecitabine tablets?

A

with/after food

115
Q

which cancer drugs can cross the BBB

A

small lipophilic drugs :
MTX
cytarabine
BCNU

116
Q

when do you need to be careful when prescribing hydrophilic drugs?

and example

A

overdosing in obese pts

e.g. doxorubicin

117
Q

why are the people with liver disease at higher risk when taking drugs?

A

poor drug metabolism due to a lack of cyto P450 = risk of toxicity

118
Q

what drugs need dose reductions in renal impairment?

A

cisplatin
carboplatin
MTX
etoposide
bleomycin

119
Q

what drugs are nephrotoxic? and how can you reduce effects?

A

cisplatin - requires adequate hydration
MTX - alkalise urine in high doses

120
Q

what drugs need dose reductions in hepatic impairment?

A

doxorubicin
vincristine
paclitaxel
etoposide

121
Q

what drugs are hepatotoxic?

A

nitrosureas - elevated liver enzymes
MTX - fibrosis/cirrhosis

122
Q

what factors determine success of chemotherapy?

A

objective of treatment
pt factors
factors related to the tumour

123
Q

what may be the overall objective of chemo treatment?

A
  • attempt to cure disease
  • focus on symptom palliation
  • choice of adjuvant chemo
124
Q

what are pt factors that effect chemo success?

A

medical condition
age
motivation
psychological status

125
Q

what are tumour factors that effect chemo success?

A

sensitivity to chemo
clinical stage/size
growth characteristics

126
Q

what are the effects of chemotherapy on various cancers?

A
  1. Often curative:
    ALL and AML, especially in children
    Testicular cancer
    Hodgkin and non-Hodgkin lymphoma Wilms’ tumour
  2. More than 30% responsive
    Breast cancer
    Small cell lung cancer
    Multiple myeloma
    CLL
  3. Usually highly resistant
    Non-small cell lung cancer
    Renal cell carcinoma
    Pancreatic cancer
127
Q

what is adjuvant chemotherapy?

A

chemo/radiotherapy given after surgery

eradicate micrometastases
low toxicity regimen

128
Q

what is neo-adjuvant chemotherapy?

A

chemo/radiotherapy given before surgery

129
Q

what is the advantage of neo-adjuvant chemotherapy?

A
  1. Earlier exposure to cytotoxic drugs
  2. Can measure objective response in primary lesion - helps determine likely success or failure of chemo.
  3. Regression of the primary tumour may allow for less extensive surgery.
130
Q

what is the disadvantage of neo-adjuvant chemotherapy?

A
  1. increased thrombocytopenia
  2. if chemo is not a success the tumour size can grow = increase surgery risk
131
Q

how are combination chemotherapy drug treatments prescribed?

A

Basic principles
1. Choose individually active drugs
2. Choose drugs with non-overlapping toxicities
3. Choose agents with different modes of action
4. Choose agents that do not display cross-resistance
5. Use drugs at their optimal dose and schedule
6. Treatment-free interval should be the shortest possible to allow recovery of most sensitive host tissue

132
Q

why are combination chemotherapy used?

A

Combinations usually more successful than single agent chemotherapy.
- prevention of resistant clones
- cytotoxicity to resting and dividing cells
- biochemical enhancement of effect

133
Q

name phase specific drugs

A

S PHASE
- cytarabine
- MTX
- 5-FU
G2 PHASE
- bleomycin
- etoposide
M PHASE
- vinca alkaloids
- paclitaxel

134
Q

name whole cell cycle specific drugs

A

Alkylating agents - chlorambucil, cyclophosphamide, cisplatin
Antibiotics - doxorubicin, epirubicin

135
Q

name cell cycle non-specific drugs

A

Nitrogen mustard
Nitrosureas - carmustine, lomustine

136
Q

what is BEP?

A

combination regimen for testicular cancer

BLEOMYCIN + ETOPOSIDE + CISPLATIN

137
Q

describe bleomycin

A

inhibits DNA synthesis
G2 phase

138
Q

what are side effects of bleomycin?

A
  • toxic to skin and mucous membranes
  • can cause pulmonary toxicity
139
Q

what are side effects of etoposide?

A
  • myelosuppressive, usually alopecia
  • moderate nausea and vomiting
  • given slowly to avoid hypotension
140
Q

what are side effects of cisplatin?

A
  • nephrotoxicity, ototoxicity, neuropathy - severe nausea and vomiting

HDT 3.2 (17 decks)

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