Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HHD 2 > Introduction to Cancer Chemotherapy > Flashcards

Introduction to Cancer Chemotherapy Flashcards

1
Q

What is cancer ?

A

This is when abnormal cell divide in an uncontrolled way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When cancers spread to other parts of the body, this is referred to as?

A

Metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

A primary tumour refers to…

A

a tumour (mass of abnormal cells) prior to metastasis and its ability to evade its tissue origins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

A secondary tumor refers to…

A

a tumour that originates from a primary tumour that has metastasised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

There are more than ____ types of cancer

A

200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the largest single preventable causes of cancer?

A

smoking
present in 15% of all cancer cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What types of cancers account for over half (53%) of new cancers?

A

Breast
Prostate
Lung
Bowel cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Age is another risk factor for the development of cancer. What evidence is there to support this?

A

Over a third (36%) of all cancer cases in the UK are diagnosed in people aged 75 and over (2016-2018)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

46% of oral cavity cancers in the UK are preventable, what lifestyle factors are linked to them?

A

smoking
betel quid
smokeless tobacco
alcohol
infections (HPV positive)
ionising radiation
sun exposure
certain occupational exposures- asbestos, inorganic acid mists, formaldehyde, wood dust, rubber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

___ % of oral cavity cancers are in HPV positive patients

A

12%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The risk of oral cavity cancer is ___% higher in current smokers compared to never smokers

A

91%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the main avoidable risk factor of oral cancer?

A

smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What factors increase the risk of developing cancer?

A

Age
Genetics
Exposure to risk factors including avoidable lifestyle factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What dietary inclusion has been found to be protective against oral cancer?

A

diet high in fruit and vegetables
insufficient fruit and vegetables are linked to an estimated 56% of oral cancer cases in the UK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the signs and symptoms of oral cancer?

A

sore mouth ulcers; do not heal within several weeks (80% of oral cancer patients)

unexplained, persistent lumps on the lip, mouth, throat and lymph glands of the neck

oral discomfort or pain that will not go away

persistent red or white patches on the lining of the mouth

difficulty when swallowing (dysphagia), chewing, moving jaw

feeling that something is caught in the throat

unusual bleeding or numbness in the mouth

loose teeth for no apparent reason or a tooth socket that does no heal

changes in voice and speech problems

unexplained weight loss

Halitosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

According to the NICE guidelines, when should a dentist consider a suspected cancer pathway referral (for an appointment within 2 weeks) ?

A

a lump on the lip or in the oral cavity consistent with oral cancer OR

a red or red and white patch in the oral cavity consistent with erythroplakia or erythroleukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does an oral squamous cell carcinoma present on the lateral border of the tongue?

A

solitary ulcer with rolled border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does an oral squamous cell carcinoma present on the ventral surface of the tongue and FoM?

A

as a red patch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does an oral squamous cell carcinoma present on the buccal mucosa?

A

speckled patch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does an oral squamous cell carcinoma present on the lower lip?

A

shallow ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In cancer, the appearance of abnormal characteristic reflect altered patterns of gene expression in cancer cells, resulting from ________ or _________ mutations

A

Inherited
Acquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give an example of a cancer type with potential inherited mutations

A

Breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give an example of a cancer type with acquired mutations

A

Oral cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the inherited mutation often implicated in breast cancer ? What is the function

A

BRCA1 and BRCA2
there are tumour suppressor genes
they are mutated and their tumour suppressor abilities are diminished; encouraging proliferation and discouraging apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What risk factors can contribute to the development of oral cancers ?

A

Exposure to viruses e.g. HPV, carcinogens (tobacco products, betel quid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is carcinogenesis?

A

This is the process by which normal cells are transformed into cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Carcinogenesis is a complex multi-stage process that involves…

A

more than one genetic change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 2 main categories of genetic change in carcinogenesis?

A

Oncogenes (protoncogenes)
Tumour suppressor genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the normal function of protoncogenes?

A

normally control cell division, apoptosis and differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Activation of protoncogenes produces …

A

oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Give an example of a protoncogene

A

c-Myc gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the normal function of tumour suppressor genes?

A

They slow down cell division, repair DNA mistakes and induce apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

In cancer cells, TSGs are ____________.

A

inactivated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Give an example of a TSG

A

TP53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Mutated TP53 genes are found in ____% of tumours

A

> 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the effect of up-regulation of oncogenes and down-regulation of TSGs?

A

induction of malignant change
cells grow out of control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is aneuploidy?

A

this is the presence of an abnormal number of chromosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What genetic changes can be observed in cancer cells?

A

chromosomal aneuploidiy
point mutations
deletions
duplications
amplifications
translocations
inversions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the karyotype of normal cells?

A

46 chromosomes
23 pairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 4 characteristics that cancer cells manifest than distinguish them from normal cells?

A

uncontrolled proliferation
de-differentiation and loss of function
invasiveness
metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

The production of what enzymes permits the invasion of nearby tissues by tumour cells?

A

metalloproteinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

_________ aids the support of metastasised tissue

A

Angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Metastasis leads to the formation of ___________ tumours

A

secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is de-differentiation ?

A

reversion to a more primitive version of the cell which can lead to a loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Name the cellular systems that can be altered in cancer cells which cause uncontrolled proliferation

A

Growth factors
Cell cycle transducers
Resistance to apoptosis
Telomerase expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Increase in which growth factor encourages angiogenesis?

A

VEGF
Vascular endothelial growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Cell cycle transducers include …

A

cyclins, cyclin dependent kinases and CDK inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How are cancer cells able to resist apoptosis?

A

inactivation of pro-apoptotic factors
Activation of anti-apoptotic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the function of telomeres?

A

protect the genetic material and allow cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What happens to telomeres with continued cell division?

A

Gets shorter which can then cause senescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the function of the telomerase enzyme?

A

to repair telomeres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Telomerase expression is ________ in cancer cells

A

increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the stages of the cell cycle?

A

Interphase; G1, S, G2
Mitosis, cytokinesis (daughter cell formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What occurs at interphase?

A

growth of the cell
There is no division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What phase of the cell cycle are most normal cells at?

A

Interphase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What occurs in G1 phase of interphase?

A

growth of cell
cellular contents (organelles), excluding the chromosomes are duplicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What occurs in the S phase of interphase?

A

duplication of chromosomes
23 pairs to 46 pairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What occurs in the G2 phase of interphase?

A

cell double checks the duplicated chromosomes for any needed repairs
preparation for mitosis

59
Q

What is the G0 phase of interphase ? What types of cells exist in this phase?

A

there is no cell division
neurones exist in this stage

60
Q

What is mitosis?

A

this is where active cell division takes place

61
Q

What are the classes of molecules that regulate the cells progression through the cell cycle?

A

Cyclins
Cyclin dependent kinases

62
Q

What activates CDKs ?

A

cyclin molecules

63
Q

Inactive CDKs are always present in the cell. True or false

A

True

64
Q

Specific cyclins are made at specific times. True or false

A

True

65
Q

What is the key checkpoint in the G1 phase of interphase. State the molecules involved an their effect.

A

cycD-CDK4 and cycE-CDK2
they phopshorylate and inactivate the Rb(retinoblastoma) protein which is a tumour suppressor. This in turn activates DNA synthesis

66
Q

What is the key checkpoint in the G1 phase of interphase. State the molecules involved an their effect.

A

cycD-CDK4 and cycE-CDK2
they phopshorylate and inactivate the Rb(retinoblastoma) protein which is a tumour suppressor. This in turn activates DNA synthesis

67
Q

What is the key checkpoint in the S phase of interphase. State the molecules involved an their effect.

A

cycA-CDK2
activates DNA replication

68
Q

What is the key checkpoint in the M phase of interphase. State the molecules involved an their effect.

A

cycb-CDK1
activation of mitosis

69
Q

What gene is referred to as the guardian of the genome?

A

p53

70
Q

What is the function of p53 protein ?

A

p53 acts as a transcription factor and binds to DNA directly
Leads to downstream activation of p21 gene

71
Q

What is the function of p21 protein?

A

complexes with CDK2 inhibiting it and prevents the cell from continuing onto cell division

72
Q

What is the effect of a mutated p53 protein/gene on the cell cycle?

A

no p21 is produced to act as a stop signal for cell division
This leads to cancer

73
Q

Mutated Rb protein/gene leads to…

A

retinoblastoma

74
Q

Cancer treatment are specifically cytotoxic to what kinds of cells?

A

rapidly dividing cells

75
Q

What is the general function of chemotherapy/anti-cancer drugs?

A

cytotoxic
most damage DNA and induce apoptosis
they are anti-proliferative

76
Q

What are the side effects of chemotherapy?

A

depress bone marrow
impair healing (platelets)
depress growth
nausea and vomiting
sterility
hair loss
teratogenecity (malformation of foetus/embryo)

77
Q

What is the mechanism of action of alkylating agents in cancer treatment ?

A

they form covalent bonds with DNA impeding DNA replication

They contain chemical groups that form covalent bonds with the nucleophilic groups in DNA

They form cabonium ion (cation)s which are attracted to nucleophilic group of DNA (mostly position N7 of guanine)

There are often 2 alkylating groups making it bifunctional

78
Q

What is a nucleophile?

A

donates an electron pair for form a bond

79
Q

What is the function of bifunctional alkylating agents?

A

they can cause intrastrand linking and crosslinking

80
Q

Alkylating agents mainly have an impact on what phase of the cell cycle?

A

S phase
affects DNA replication
unpaired DNA is more susceptible

81
Q

Where are nucleophilic groups of DNA mostly found ?

A

N7 position of guanine

82
Q

What are the side effects of alkylating agents?

A

depress bone marrow function
cause hair loss
GI disturbances
increased risk of acute non-lymphocytic anaemia (fast growing myeloblasts)

83
Q

What is the effect of prolonged use of alkylating agents?

A

gametogenesis
Sterility particularly in men

84
Q

Give examples of alkylating agents

A

nitrogen mustards
nitrosoureas
platinum compounds
other

85
Q

Give an example of a nitrogen mustard

A

cyclophsophamide

86
Q

What are some side effects of cyclophosphamide?

A

nausea and vomiting
bone marrow depression
haemorrhagic cystitis (lining of bladder becomes inflammed and starts to bleed)
immunosuppressant (affects lymphocytes)

87
Q

Cyclophopshamide is a prodrug which is converted in the liver by ______

A

P450 enzymes

88
Q

Give examples of nitrosoureas

A

Lomustine
Carmustine

89
Q

What are the side effect of nitrosureas?

A

severe bone marrow depression

90
Q

Nitrosoureas can be used to treat brain tumours because…

A

they are lipid soluble and thus can cross the BBB

91
Q

What are side effects of other alkylating agents such as decarbazine ?

A

myelotoxicity
severe nausea and vomiting

92
Q

Decarbazine is a prodrug and is activated in the liver by P450. True or false

A

True

93
Q

How do platinum compounds differ from other alkylating agents?

A

they do not have carbonium ions
they have ethylene ammonium (lose chloride ions)

Ethylene ammonium is unstable

94
Q

Give an example of a platinum compound

A

cisplatin

95
Q

What are the side effects of platinum compounds?

A

severe nephrotoxicty
severe nausea and vomiting
peripheral neuropathies
ototoxicity (hearing or balance problems due to medication)

96
Q

Platinum compounds are revolutionised for treating what kinds of tumours?

A

revolutionised treatment of germ cell tumors

97
Q

What is the MOA of antimetabolites ?

A

they disrupt the metabolic pathways involved in DNA synthesis
disruption of nucleotide bases?

98
Q

What is the MOA of methotrexate?

A

Methotrexate inhibits the action of DHFR (dihydrofolate reductase) enzyme

methotrexate is an antagonist of folate (prevents formation of FH4) therefore interfering with the action of thymidylate synthetase

99
Q

Briefly state how dTTP (pyrimidine base- thymidine) is formed

A

DHFR reduces folates to tetrahydrofolate (FH4)

FH4 acts as a co-factor (methyl group donor) necessary for the conversion of dUMP to dTM by the enzyme thymidylate synthase (TS)

dTMP can then be phosphorylated to form the pyrimidine base dTTP (thymidine) which is required for DNA synthesis

100
Q

What is the MOA of fluorouracil?

A

Inhibits the action of thymidylate synthetase (prevents production of dTMP from dUMP)

it is a pyrimidine (thymine, uracil, cytosine) analogue; a fraudulent nucleotide which binds to and inhibits thymidylate synthase

101
Q

How is methotrexate resistance developed?

A

pumps on the cell surface can pump out methotrexate

102
Q

Methotrexate can also be used as an ______________ drug?

A

immunosuppresant

103
Q

What are the side effects of methotrexate?

A

bone marrow depression
damage to GI tract epithelium
pneumonitis
nephrotoxicity (high doses)

104
Q

What are the side effects of fluorouracil?

A

damage to GI tract epithelium
myelotoxicity

105
Q

Give an example of a purine analogue ? What is their function

A

Mercaptopurine
they can disrupt other pathways involved in DNA synthesis

106
Q

What is the mechanism of action of cytotoxic antibiotics?

A

they often have direct action on DNA

107
Q

What is the function of the topisomerase enzyme?

A

encourages DNA unwinding
prevents DNA tangling by cutting through one strands of the DNA molecule
The unbroken strand then goes through the broken strand thus untangling the protein molecule.

108
Q

What is doxorubicin?

A

an anthracycline antibiotic derived from the streptomyces bacterium

109
Q

What is the MOA of doxorubicin?

A

they bind to DNA and inhibit DNA and RNA synthesis
They do this by stabilising the topoisomerase II-DNA complexes that are easily cleaved or it interferes with its catalytic activity

this results in double stranded breaks in DNA (easily cleaved state)
this causes arrest in the cell cycle at the G2 phase

110
Q

What are the side effects of cytotoxic antibiotics

A

myelosuppression
hair loss
cardiotoxic in high doses
nausea and vomiting

111
Q

What is the relevance of the plant derivative (mandrake root) Etoposide in cancer therapy?

A

it is thought to an an effect on topoismerase II similar to doxorubicin although this remains unclear

112
Q

Give examples of hormone sensitive tissues

A

Breast
Uterus
Prostrate

113
Q

What is the rationale for the use of hormone antagonists in cancer therapy ?

A

tumours that arise in hormone sensitive tissues may be hormone dependent due to the presence of hormone receptors on these malignant cells

Their growth ca therefore be inhibited by hormone antagonists or the inhibition of hormone synthesis

114
Q

What is the MOA of tamoxifen?

A

an anti-oestrogen; oestrogen antagonist
it competes with endogenous oestrogen for the oestrogen receptors inhibiting the transcription of oestrogen responsive genes

115
Q

What is the MOA of anastrozole?

A

it is an aromatase inhibitor
oestrogen is synthesised from androgens in the adrenal cortex, either immediately (androstenedione) or through testosterone both catalysed by the enzyme aromatase

116
Q

What kind of cancer is anastrozole used to treat?

A

Post-menopausal breast cancer
Anastrozole inhibits aromatase, suppressing oestrogen synthesis

117
Q

What are the common side effects of tamoxifen (competitive oestrogen antagonist)?

A

light headed
hot flushes and sweats
nausea and vomiting
tiredness or fatigue
irregular periods
hair thinning

118
Q

What are the rare side effects of tamoxifen?

A

Tumor flare (bone pain, if cancer has spread there)
skin rash
liver changes
risk of blood clots (thrombosis)
increased risk of developing womb cancer

119
Q

What are the common side effects of anastrozole?

A

headaches
hot flushes and sweats
nausea and vomiting
tiredness or fatigue
mood changes
skin rashes

120
Q

What are the rare side effects of anastrozole?

A

tumour flare- bone pain if the tumour has spread there
hair thinning
liver changes
diarrhoea
vaginal bleeding

121
Q

What is the rationale for the use of monoclonal antibodies and protein kinase inhibitors in cancer therapy?

A

many tumours overexpress growth factors, stimulating cell proliferation and tumour growth

122
Q

What is the MOA of monoclonal antibodies?

A

they bind to growth factor receptors or bind to and neutralise growth factors

123
Q

Give examples of monoclonal antibodies that bind to growth factor receptors?

A

Transtuzumab
Cetuximab

124
Q

Give examples of monoclonal antibodies that bind to and neutralise growth factors?

A

bevacizumab

125
Q

What is the function of imatinib?

A

monoclonal antibody that prevents downstream signalling triggered by growth factors by inhibiting specific oncogenic kinases

126
Q

List some side effects of trastuzumab

A

Anaemia
Alopecia
constipation
dry eyes
cystitis (inflammation and bleeding of the bladder)
hypersensitivity

127
Q

List some side effects of cetuximab

A

decreased appetite
hypersensitivity
nausea
eye inflammation
interstitial lung disease

128
Q

List some side effects of bevacizumab

A

abscess
anaemia
constipation
hypersensitivity
arthalagia
vomiting

129
Q

Lis some side effects of imatinib

A

dysphagia
drowsiness
dizziness
anxiety
arrhythmias

130
Q

What is primary resistance to cytotoxic drugs?

A

resistance that is present when the drug is first administered

131
Q

What is acquired resistance to cytotoxic drugs ?

A

resistance that is through adaptation or mutations during drug treatment

132
Q

What is the mechanism for resistance to doxorubicin?

A

decreased accumulation of cytotoxic drug; increased expression of cell surface pumps

133
Q

What is the mechanism for resistance to methotrexate?

A

a decrease in the amount of drug taken up

134
Q

What is the mechanism for resistance to fluorouracil, mercaptopurine?

A

insufficient activation of the drug

135
Q

What is the mechanism for resistance to mercaptouring?

A

increase in inactivation

136
Q

What is the mechanism for resistance to methotrexate?

A

increase the concentration of the target enzyme
DHFR- dihydrofolate reductase

137
Q

What is the mechanism for resistance to antimetabolites?

A

increased utilisation of other metabolic pathways

138
Q

What is the mechanism for resistance to alkylating agents

A

rapid repair of drug induced DNA damage

139
Q

What is the mechanism for resistance to doxirubicin?

A

altered activity of the target (topoisomerase II)

140
Q

What is the mechanism for resistance to P53 agents?

A

mutation of various other genes

141
Q

What are some oral complications related to chemo and radiotherapy?

A

oral bleeding due to bone marrow effects
oral mucositis (inflammation of mucosa)
infection
salivary gland dysfunction
dental decay
changes in perception of food
abnormal dental development (children)
osteonecrosis
poor nutrition
functional disabilities
neurotoxicity

142
Q

What is the implication of increased risk of bleeding and infections due to cancer therapy in dental treatment?

A

surgical procedures such as extractions should be avoided

143
Q

What is the implication of drug to drug interactions with cancer therapy?

A

consult BNF or discuss with patients oncologist if there is any doubt about prescribing another medication

HHD 2 (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions