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Pharmacology > Anti-Cancer Drugs > Flashcards

Anti-Cancer Drugs Flashcards

1
Q

what is cancer?

A

a group of diseases involving abnormal cell growth with the potential to invade or to spread to other parts of the body
leading cause of death in Canada

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2
Q

what are the top three types of cancers in females? in males?

A

female: breast, lung, colorectal
male: prostate, colorectal, lung

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3
Q

what age category is affected most by cancer? name an exception

A

older people

exception: testicular

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4
Q

what are 4 different fates of a cell?

A

stem cell renewal
differentiation
growth/quiescence
death

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5
Q

what occurs in cancerous cells regarding cell division?

A

unregulated cell division
can go on to be benign (non-cancerous; no effect on surrounding tissue) or malignant (cancerous; invades surrounding tissue)
a cell can also break away and start a new tumour elsewhere (metastasis)

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6
Q

what causes a cell to have uncontrolled cell division?

A

accumulation of a group of mutations that are enough to overdrive cell division

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7
Q

what are 7 hallmarks of cancer?**

A

1) self-sufficiency in growth signals
2) insensitivity to anti-growth signals
3) evading apoptosis
4) limitless reproductive potential
5) sustained angiogenesis
6) tissue invasion and metastases
7) genomic instability

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8
Q

what kind of mutations would occur that could affect cell growth?

A

1) deactivate DNA repair
2) inactivate tumour suppressor genes
3) activate pro-oncogenes

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9
Q

what is the minimum amount of gene mutations that usually occurs when cancer is formed? how many often occur?

A

5 mutations

often 6-9

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10
Q

is cancer hereditary?

A

no, but we can inherit dispositions (susceptibility) to cancer

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11
Q

what increases the frequency of cancer?

A

increases in mutation rate or genomic instability

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12
Q

what is aneuploidy?

A

presence of abnormal number of chromosomes in the cell

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13
Q

what are some inherited cancer syndromes?

A

p53, BRCA1 and 2, MMR (mismatched pair)

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14
Q

what factors can influence the genetic/developmental component of etiology of cancer?

A

inherited cancer syndromes
immune deficiency syndromes (enhanced predisposition)
polymorphisms (influence risk, occurrence, progression, and treatment)

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15
Q

what factors can influence the nurture component of etiology of cancer?

A 
radiation
chemotherapy
viruses and bacteria (H. pylori, EBV)
repeated injury (acid reflux, hepatitis)
workplace/home exposures
other environmental/lifestyle factors
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16
Q

what are some environmental factors that influence the etiology of cancer?

A

food additives (nitrites)
pollution (asbestos)
occupational (benzene)
industrial (hydrocarbons - soot)

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17
Q

what lifestyle factors influence the etiology of cancer?

A

tobacco
alcohol
diet (obesity)
viruses (HPV, HIV)

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18
Q

what initiator-promoter situations would lead to cancer? which wouldnt?

A

cancer:
initiator first shortly followed by promoter
initiator followed by a promoter later on
no cancer:
promoter comes before the initiator
initiator followed by little promotions throughout

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19
Q

what are tumour initiators?

A

mutagens; x rays, ultraviolet light, and DNA alkylating agents

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20
Q

what are tumour promoters?

A

proliferation inducers; phorbol esters, inflammation, alcohol, estrogen and androgens, EBV

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21
Q

describe dysregulated cell cycle in cancer?

A

cells divide when they are not supposed to

cells divide in a place they are not supposed to

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22
Q

what are the 5 phases of cell cycle?

A 
G1
S
G2
M
G0
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23
Q

what is the G1 phase?

A

gap phase

cell grows and prepares to synthesizes DNA

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24
Q

what is the S phase?

A

synthesis phase

cell synthesizes DNA

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25
Q

what is the G2 phase?

A

second gap phase

cell prepares to divide

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26
Q

what is the M phase?

A

mitosis phase

cell division occurs

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27
Q

what is the G0 phase?

A

arrest/quiescent phase

cell is in a resting state

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28
Q

what are the 3 different checkpoints in cell cycle?

A

G1/S checkpoint - cell monitors size and DNA integrity
G2/M checkpoint - cell monitors DNA synthesis and damage
M checkpoint - cell monitors spindle formation and attachment to kinetophores

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29
Q

what are two different protein complexes involved in the cell cycle?

A

cyclins - levels change throughout cell cycle

cyclin dependent kinases - stable levels

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30
Q

what is the function of cyclins and Cdks?

A

ability to drive through the checkpoints in cell cycle

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31
Q

how do Cdks work?

A

bind to correct cyclin in order to function
act as kinases (add phosphate group) and convert them from an off to an on state
cause a cascade of kinases adding phosphates to other proteins to activate them, that eventually leads to transcription of genes (transcription factors)

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32
Q

what is the normal function of oncogenes?

A

cell growth and gene transcription; drive cell cycle
other common functions: growth factors, growth factor receptors, signal transducers nuclear receptors, transcription factors, anti-apoptotic factors

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33
Q

what is the normal function of tumour suppressor genes?

A

DNA repair, cell cycle control, cell death

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34
Q

what are oncogenes?

A

a gene, that when mutated gains a function or is expressed at abnormally-high levels and/or high activity (often kinases, transcription factors or growth factors/receptors)

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35
Q

what are tumour suppressor genes?

A

encodes for a protein that is involved in suppressing cell division and when mutated, it is no longer functional

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36
Q

what is often the first mutation in developing cancer?

A

mutation to tumour suppression genes

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37
Q

what is p53?

A

a classic tumour suppressor (50% of all cancer from p53 mutation)

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38
Q

what does p53 do?

A

senses genomic damage (via ATM) and halts the cell cycle and initiates DNA repair
if DNA is irreparable, it will initiate the cell death process

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39
Q

what is Rb and what does it do?

A

a classic tumour suppressor
binds to a protein (E2F1) that inhibits the function of E2F1 (G1/S cell cycle transition)
ie: crucial cell cycle checkpoint

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40
Q

what is HER2/neu? what type of cancer is it typically associated with?

A 
amplified oncogene; a growth factor receptor
breast cancer (25-30% of cancer cases over-express it)
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41
Q

what is the treatment against HER2/neu?

A

Herceptin - binds to and inhibits function of receptor

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42
Q

what is Ras?

A

a frequently mutated oncogene; a growth factor receptor

transduces multiple cell signals

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43
Q

which oncogene is the most common to be mutated?

A

Ras gene

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44
Q

what happens when Ras is mutated?

A

signal-independent hyperactivation of expression, cell proliferation, and anti-apoptotic signalling

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45
Q

what are some examples of a DNA repair defect? why are they significant?

A 
base modification
Single strand break
bulky lesion
cross-link of base pairs
double strand break
95% of all cancers have at least 1 or more DNA repair defects
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46
Q

what kind of defects can happen to the chromosome to cause genomic instability?

A

gross translocations

loss/gain of chromosome parts

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47
Q

what is the difference between pseudodiploid and hyperdiploid?

A

pseudo - 2 RNA genomes per virion but give rise to 1 DNA copy in the infected cell
hyper - more than a diploid number of chromosomes

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48
Q

what is the difference between early and late stages of tumour growth?

A

early - high growth fraction; short doubling time

late - low growth fraction; long doubling times

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49
Q

when is chemotherapy most effective?

A

high growth fraction

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50
Q

define the following terms:
carcinoma
sarcoma
leukemia/lymphoma/myeloma

A

carcinoma - epithelial
sarcoma - mesenchyme
leukemia etc - hematopoietic

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51
Q

what is hyperplasia?

A

increased number of cells

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52
Q

what is hypertrophy?

A

increased size of cells

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53
Q

what is dysplasia?

A

disorderly proliferation

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54
Q

what is neoplasia?

A

abnormal new growth

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55
Q

what is anaplasia?

A

lack of differentiation

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56
Q

what are some examples of carcinoma?

A 
lung
breast
colon
bladder
prostate
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57
Q

what are some examples of sarcoma?

A

fat
bone
muscle

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58
Q

what are the 4 stages of tumour progression?

A

1) hyperplasia
2) dysplasia
3) carcinoma in situ (does not cross basal lamina)
4) cancer (malignant tumours)

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59
Q

what are 4 differences between benign and malignant tumours?

A 
benign (non-invasive):
- well defined borders
- well differentiated
- regular nuclei
- rare mitoses
malignant (invasive/metastatic):
- irregular borders
- poorly differentiated
- irregular, large nuclei
- more frequent and/or abnormal mitoses
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60
Q

what are two ways of predicting the behaviour of the tumour?

A

grade - how bad do the cells look

stage - where has the cancer spread?

61
Q

what are the 3 factors used to determine the stage of the cancer?

A

tumour - size (less than 2 cm = stage 1)
nodes (lymph) - number of lymph nodes overtaken by the tumour?
metastases - number of metastatic sites

62
Q

what are the 4 grades of cancer?

A

grade 1 - well differentiated
grade 2 - moderately differentiated
grade 3 - poorly differentiated (most loss of structure)
grade 4 - anaplastic (no structure, completely abnormal)

63
Q

what are some methods used to detect tumours>

A 
blood work
palpation
symptomatic
CT scan
PET/CT
SPECT/CT
MRI
64
Q

what is the cure rate for surgery and/or radiation? cure rate for chemo alone?

A

surg - 30%

chemo - 10-15%

65
Q

what are the possible therapeutic routes for cancer?

A 
surgery
radiotherapy
chemotherapy
immunotherapy
biologic therapy (vaccines, gene therapy)
66
Q

what are some factors that determine what kind of cancer treatment you would use?

A

type of tumour
location and amt of disease
health status of patient

67
Q

what is the objective for cancer treatment?

A

to kill cancer cells and/or lead them to apoptosis

contain and/or limit cell growth

68
Q

how does growth fraction affect outcome of cancer treatment?

A

determines efficacy of CCS drugs

69
Q

what is growth fraction?

A

percent of cells not in G0 phase

70
Q

how does doubling time affect the outcome of cancer treatment/

A

affects course scheduling

71
Q

how does the type and stage of cancer affect outcome of treatment?

A

can determine whether they will cure the cancer or palliation

72
Q

how does resistance affect the outcome of cancer treatment?

A

can limit treatment and/or force a switch in medication

73
Q

how does bone marrow capacity of the patient affect outcome of cancer treatment?

A

bone marrow suppression is the major dose-limiting toxicity for many drugs, so capacity will determine both dose and duration of treatment

74
Q

how does liver and kidney function of the patient affect outcome of cancer treatment?

A

many antineoplastic drugs are metabolized in the liver and/or eliminated in the urine, so liver and kidney function will determine drug selection and/or dosage

75
Q

how does patient compliance affect outcome of cancer treatment?

A

effects of many cancer drugs are so severe that patients will choose to stop treatment (ex: N/V)

76
Q

what are the different cells affected by cytotoxicity?

A 
cancer cells
bone marrow cells
GI mucosa (N/V)
hair follicles (alopecia)
taste buds (dysgeusia)
fetus (CI'd in pregnancy)
77
Q

what is radiation recall reaction?

A

erythema and desquamation of the skin at sites of prior radiation therapy
ie: rash and skin peeling
mostly associated with anthracycline antibiotics (doxorubicin)

78
Q

what type of cancers are classified under palliative therapy?

A

lung
esophogial
pancreatic
most brain tumours

79
Q

what is radiation?

A

ionization and excitation of atoms that kill cells

80
Q

what are some side effects to radiation?

A 
nausea vomiting
fatigue
somnolence
later: fibrosis, gliosis
skin/mucosal reactions are accentuated by other modalities like chemotherapy
81
Q

what are the different kinds of radiation?

A

external beam radiation - gamme photons and neutron beams
radioimmunoconjugates - antibody targeted radiation
radioconjugates - isotope tagged to bone seeking material
free isotopes - 131I, gallium

82
Q

what are the purposes for chemotherapy?

A

primary purpose is to shrink or eliminate tumours
neoadjuvant - make tumour more amenable to other therapies
adjuvant - eradicate micro metastasis
palliation - symptom control

83
Q

what are phase specific agents of chemotherapy?

A

schedule dependent;
more effective when given in divided doses at repeated intervals
more effective in tumours with high growth fraction
ex) Vinca alkaloids, antimetabolites

84
Q

what are phase non-specific agents of chemotherapy?

A

exert effects throughout the cell cycle
dose or concentration dependent effects
may have effect in resting phase
ex) doxorubicin, cisplatin

85
Q

what is the fraction-kill hypothesis?

A

tumour accumulates between cycles
therefore cancer chemotherapeutics are typically given in cycles to allow normal cells time to recover from treatment
chemotherapy follows exponential log kill (never reaches zero)
this also allows remaining cancer cells to recover and develop resistance

86
Q

what is tumour heterogeneity?

A

most tumours don’t have just one homogenous cell type

leads to resistance

87
Q

what are some differences between cell cycle specific and non-cell cycle specific agents?

A

CCS:
primary action only during specific phase of the cell cycle (ex: plant alkaloids G2-M; DNA synthesis S)
only proliferating cells killed (high growth factor tumours preferentially eliminated)
schedule dependent (duration and timing rather than dose)
NCCS:
any phase, including G0, although final toxicity may be manifested during a specific phase (Crosslinking agents, anthracycline antibiotics)
both proliferating and non-proliferating cells killed (attack both high and low growth factor tumours)
dose dependent (total dose rather than schedule)

88
Q

how can we reduce the impact of the recovery/resistance problem outlined in the fraction-kill hypothesis?

A

use high doses (including increasing doses during treatment, called dose escalation)
minimize recovery intervals
employ sequential scheduling during combination therapy

89
Q

what are critical factors to treatment regarding the fraction-kill hypothesis?

A

early start to treatment
treatment must continue past the time when cancer cells can be detected using conventional techniques
appropriate scheduling of treatment courses and care to ensure that a sufficient log-kill is obtained are also crucial factors that enable success

90
Q

what are the three stages where chemo works?

A

1) inhibitors of cell growth (Growth factor proteins)
2) inhibitors of DNA duplication
3) inhibitors of cell division

91
Q

give some examples of genotoxic agents (NCCS)

A 
cisplatin
carboplatin
oxaliplatin
daunorubicin
doxorubicin
epirubicin
idarubicin
cyclophosphamide
ifosfamide
92
Q

what do genotoxic agents?

A

affect the function of nucleic acids
binds directly to DNA and inhibit DNA replication enzymes
DNA damage leads to apoptosis

93
Q

describe the MoA for genotoxic agents

A

alkylation of DNA bases (disrupts base pair action - forces strand to fall apart)
creation of inter/intra-strand DNA cross links (cannot be pulled apart; inhibit replication)
induce mispairing of nucleotides (change how base looks, induces different type of base pairing effects)

94
Q

what are the most commonly used genotoxic agents?

A 
cisplatin
carboplatin
oxaliplatn
doxorubicin analogs
cyclophosphamide (prodrug; orally active; less side effects in normal cells)
95
Q

what are some adverse effects of commonly used genotoxic agents?

A

hematopoietic effects; GI; hair loss
associated with increased risk of developing cancer
renal toxicity/ototoxicity with cisplatin
heart effects with doxorubicin based cpds (cardiomyopathy/CHF)
bladder effects with cyclophosphamide cpds hemorrhagic cystitis

96
Q

what are antimetabolites?

A

structurally similar to natural metabolites and prevents cells from carrying out vital functions and they are unable to grow and survive
they interfere with the production of nucleic acids, RNA, and DNA
works in the S phase

97
Q

what are some examples of antimetabolites?

A

folate antagonists
purine antagonists
pyrimidine antagonists

98
Q

what is an example of a folate antagonist? how do they work?

A

methotrexate
inhibits dihyrdofolate reductase (an enzyme involved in the formation of purine and pyrimidine nucleotides for DNA synthesis)

99
Q

what is pemetrexed?

A

next generation antifolate
inhibits DHFR, thymidylate synthase, and glycinamide ribonucleotide formyl transferase (GRFT)
more effectively inhibits DNA and RNA synthesis

100
Q

what is folinic acid used for?

A

adjuvant
used with methotrexate and antifolates to reduce (rescue therapy) myelosuppression (often the most significant dose limiting adverse reaction)
it is a THF analog that can be used as a methyl donor

101
Q

what are some examples of purine antagonists? how do they work?

A

6-mercaptopurine - adenine
6-thioguanine - guanine
look very similar to these purines
prevents continued replication of DNA (purines are chemicals used to build the nucleotides of DNA and RNA)

102
Q

what is thiopurine methyltransferase?

A

catalyzes the S-methylation of thiopurine drugs
metabolizes azathioprine, 6-mercaptopurine, and 6-thioguanine
defects in the TPMT gene leads to decreased methylation and decreased inactivation of 6MP, leading to enhanced bone marrow toxicity which may cause myelosuppression, anemia, bleeding tendency, leukopenia, and infection
90% of population are extensive metabolizers; 10% intermediate metabolizers and rarely there are poor metabolizers

103
Q

what are pyrimidine antagonists?

A

block the synthesis of pyrimidine containing nucleotides (dCTP and dTTP in DNA; CTP and UTP in RNA) and stops DNA/RNA synthesis, meaning cell division is inhibited
look very similar to pyrimidines

104
Q

name some examples of pyrimidine antagonists

A

5-fluorouracil

cytarabine (cytosine arabinoside)

105
Q

what is the MoA for 5-FU?

A

acts as an antimetabolite irreversibly inhibits TS by competitively binding
inhibits conversion of dUMP to dTMP

106
Q

What is the main cancer treated by 5-FU?

A

colorectal cancer

107
Q

what is the mitotic spindle?

A

attaches to kinetochores, helps align chromosomes and then separates them

108
Q

what are MAD and BUB?

A

part of the spindle checkpoint that halt the cell cycle until all chromosomes are aligned at the middle of the cell

109
Q

what are cytoskeletal inhibitors?

A

affect the mechanics of cell division

without proper microtubule formation, cell division cannot occur

110
Q

what are two classes of cytoskeletal inhibitors? give some examples of drugs from each class

A

vinca alkaloids:
vincristine, vimblastin, vindesine
taxanes:
paclitaxel, docetaxel

111
Q

how do vinca alkaloids and taxanes differ?

A

vinca: affects metaphase, affects polymerization
taxanes: affects anaphase, affects depolymerization

112
Q

what are some side effects of vinca alkaloids?

A 
loss of WBCs and blood platelets
GI problems
high BP
excessive sweating
depression
muscle cramps
vertigo
headaches
peripheral neuropathy
hyponatremia
constipation
hair loss
113
Q

what are some side effects of taxanes?

A 
nausea/vomiting
loss of appetite
thinned/brittle heair
pain in joints of arms or legs lasting two to three days
changes in color of nails
tingling of hands/toes
bruising or bleeding
hand-foot syndrone
fever
chills
cough
sore throat
difficulty swallowing
dizziness
shortness of breath
severe exhaustion
skin rash
facial flushing
female infertility (ovarian damage)
114
Q

what are topoisomerase inhibitors?

A

work in G2 phase
interfere with the action of topoisomerase enzymes (I and II) which are enzymes that control the changes in DNA Structure by catalyzing the breaking and rejoining of the phosphodiester backbone of DNA strands during the normal cell cycle (help in the unwinding/relaxing of DNA Strands)
blocks the ligation step of the cell cycle, generating single and double stranded breaks that harm the integrity of the genome = apoptosis and cell death

115
Q

what are some examples of topoisomerase I inhibitors? what step do they work at?

A

topotecan
irinotecan
cut 3’ end under other strand and reseal DNA

116
Q

what are some examples of topoisomerase II inhibitors?

A

etoposide

teniposide

117
Q

what are the 5 steps of steroid hormone action in the cell?

A

1) steroid hormone enters cell
2) hormone binds to receptor, induces conformational change
3) hormone-receptor complex binds to DNA, induces start of transcription
4) many mRNA transcripts are produced, amplifying the signal
5) each transcript is translated many times, further amplifying the signal

118
Q

what is hormone therapy?

A

a type of therapy where you starve cancer cells from hormonal signals necessary for growth
use hormone blocking drugs at target cell and prevent hormone production

119
Q

what are 3 types of hormonal antagonists?

A 
selective estrogen receptor modulators (SERMs)
aromatase inhibitors (AI)
selective androgen receptor modulators (SARMs)
120
Q

what are SERMs? give some examples of drugs

A 
cause changes in gene expression, preventing cell division; inhibits estrogen's growth stimulating effects
drugs:
tamoxifen
raloxifen
toremifen
121
Q

what is the primary active metabolite of tamoxifen?

A

endoxifen via CYP2D6

122
Q

how do CYP2D6 polymorphisms affect tamoxifen effects?

A

lower activity can reduce endoxifen formation and drug effectiveness
can interact with antidepressants which can reduce endoxifen levels

123
Q

what do aromatase inhibitors do? give some examples

A

prevents hormone formation
exemestane
anastrozole
letrozole

124
Q

what do SARMs do? give some examples

A

competitively bind to the androgen receptor
flutamide
bicalutamide

125
Q

what are the benefits of combination therapy?

A

synergistic effects at lower doses with decreased toxicity
decreased development of resistance
broader cell kill in cancers that consist of a heterogeneous tumour cell population

126
Q

what are some adverse side effects of chemo drugs?

A

bone marrow depression - anemia, bleeding, infections, secondary cancers
teratogenesis
carcinogenesis
resistance

127
Q

how does cancer develop resistance to methotrexate?

A

increased concentrations of CHFR enzyme in cancer cells (gene amplification)

128
Q

what are some resistance mechanisms to chemotherapy?

A

increased expression of target proteins
failure of drugs to enter cancer cells or increased rate of removal of drug from cancer cell
drugs fail to reach target cells
target molecule is no longer present
target molecule is altered (mutation/deletion)
often is a combination of these

129
Q

what is p-glycoprotein and what is its role in resistance?

A

is a transmembrane ATP-dependent efflux pump that actively transports many types of chemotherapy from cells (anthracyclines, vinca alkaloids, taxanes)
first multidrug resistance mechanism to be characterized; overexpression in cancers causes drug resistance

130
Q

what is the major cause of multidrug resistance?

A

failure of DNA damaged cells to undergo apoptosis which typically occurs because of oncogenic mutations

131
Q

what are immuno-modulators? what are some SEs?

A

modify the immune system response and are primarily used in hematopoietic neoplasias
SE’s: flu like sx, fever and capillary leak syndrome (severe)

132
Q

name three drugs classified under monoclonal antibody therapy?

A

rituximab
trastuzumab
cetuxmab

133
Q

what does rituximab do?

A

binds to CD20 antigen receptor present on the cell surface of B lymphocytes, targeting the cell to complement-activated phagocytosis and antibody-dependent apoptosis
results in inhibited proliferation of lymphocytes and lymphoma cells

134
Q

what are some SE’s to rituximab?

A

severe hypersensitivity reactions

anaphylaxis

135
Q

what does trastuzumab do?

A

binds to human epidermal growth receptor protein 2 (HER2) which is over-expressed in some cancers (breast); associated with faster growth and higher relapse

136
Q

what are some SE’s to trastuzumab?

A

allergic reactions
heart muscle damage (heart failure)
pulmonary toxicity

137
Q

what does cetuximab do?

A

chimeric monoclonal antibody against epidermal growth factor receptor protein (EGFR) which is overexpressed in some cancers

138
Q

what are some SE’s to cetuximab?

A 
acne
fever
chills
hypotension
bronchospasm
dyspnea
wheezing
angioedema
anaphylaxis
cardiac arrest
139
Q

what is imatinib?

A

selective tyrosine kinase inhibitor

prevents phosphorylation of specific proteins involved in cell growth and differentiation

140
Q

what does gefitinib do?

A

interrupts mutated or overactive EGFR receptor signalling

141
Q

what is erlotinib?

A

reversible EGFR tyrosine kinase inhibitor, with similar MoA as gefitinib

142
Q

what are 2 benefits to using imatinib, gefitinib, or erlotinib?

A

fewer side effects

target is much more selective for tumour cells

143
Q

what are antibody-drug conjugates? what is a benefit to using them?

A

combines properties of monoclonal antibodies with cytotoxic small molecule drugs
allows discrimination between healthy and diseased tissue

144
Q

what is brentuximab vedotin?

A

antibody-drug conjugate

Anti-CD30 monoclonal antibody with anti-mitotic monoethyl auristatin E; blocks microtubule formation

145
Q

what are some side effects to brentuximab vedotin?

A 
peripheral neuropathy
neutropenia
fatigue
nausea/vomiting
anemia
upper RT infection
diarrhea
fever
rash
thrombocytopenia
cough
black box warning: progressive multifocal leukoencephalopathy (PML)
146
Q

what is trastuzumab emtansine?

A

anti-HER2 monoclonal antibody combined with anti-mitotic mertansine; inhibits microtubule polymerization

147
Q

what are some side effects to trastuzumab emtansine? which are common and which are rare?

A 
common:
fatigue
nausea
musculoskeletal pain
thrombocytopenia
headache
increased liver enzyme levels
constipation
rare:
hepatotoxicity
liver failure
hepatic encephalopathy
nodular regenerative hyperplasia
heart damage
interstitial lung disease
thrombocytopenia
peripheral neuropathy
148
Q

what is bevacizumab? what are some advantages and disadvantages?

A

new generation chemotherapeutics
targets new endothelial cell growth into the tumour (Angiogenesis inhibitors)
pros: fewer side effects, less chance of resistance
cons: angiogenesis is important in wound healing and normal development, long term effects of treatment yet unknown

Pharmacology (9 decks)

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