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CAN > L08: Chemotherapy Mechanims Of Action > Flashcards

L08: Chemotherapy Mechanims Of Action Flashcards

1
Q

What are the 3 main modalities of treating cancer

A

Surgery
Radiotherapy
Chemotherapy

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2
Q

What treatment modality does cytotoxic drugs belong to

A

Chemotherapy

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3
Q

What is the therapeutic index of cytotoxic drugs like

A

Narrow

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4
Q

What does a narrow therapeutic index mean

A

Agents that target the diving cells (tumour cells) can affect normal healthy cells that are also dividing

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5
Q

Can normal cells recover from cytotoxic injury

A

Yes

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6
Q

What structures and cells does cytotoxic drugs affect

A 
Bone marrow 
GIT
Germinal epithelium 
Lymphoid tissue 
Hair follicles
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7
Q

Are cytotoxic drugs targeted drugs

A

No

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8
Q

If cytotoxic drugs are not targeted drugs what vital organs can they affect

A

Kidney
Nerves
Heart
Lungs

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9
Q

What can the affect of cytotoxic drugs on these organs cause

A

Renal failure
Nerve damage
Heart failure
Lung fibrosis

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10
Q

What does genotoxic mean

A

Toxic (Damaging) to DNA

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11
Q

Are cytotoxic drugs genotoxic

A

Yes

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12
Q

If cytotoxic drugs are genotoxic what can this lead to

A

Mutations

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13
Q

What can mutations in people using cytotoxic drugs result in overall

A

Secondary malignancy

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14
Q

When increasing the dose of cytotoxic drugs to get an anti cancer effect what chance also increases

A

Toxicity

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15
Q

What are the 10 hallmarks of cancer

A

1) sustaining proliferative signalling
2) evading growth suppressors
3) enable replicative immortality
4) resisting cell death
5) activating invasion and metastasis
6) inducing angiogenesis
7) deregulating cellular energetic
8) avoiding immune destruction
9) tumour promoting inflammation
10) genome instability and mutation

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16
Q

If we know the hall marks of cancer what can we do

A

Molecular target and engineer drugs that hit those targets

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17
Q

Which patients is molecular targeted drugs likely to work on

A

Specific patients based on the molecular properties of cancer

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18
Q

Compare cytotoxic drugs and molecules targeted drugs in terms of the cancer they can target and toxicity

A

Cytotoxic drugs: effective against a broad number of cancer, but toxic
Molecular targeted drugs: effective against specific cancer and less toxic

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19
Q

What does cytotoxic drugs work on in the cell

A

Cell cycle

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20
Q

How do different agents work on the cell cycle

A

Different agents have different effects on the cell cycle

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21
Q

Name the different cytotoxic drugs that we use

A 
Micro-tubule inhibitors 
Topoisomerase inhibitors 
Alkylating agents 
Anti-metaboliities
Platinum analogues
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22
Q

What is p53

A

A tumour suppressor gene

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23
Q

When there is cytotoxic damage what happens to P53

A

Plays a role in detecting cytotoxic and genotoxic damage then transcriptional activator to mediate G1, G2 cell cycle arrest or apoptosis

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24
Q

In many cancers what is p53 like

A

Lost or mutated so it is inactive

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25
Q

In chemotherapy what are we trying to trigger

A

Apoptosis

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26
Q

What are the 2 pathway of apoptosis

A

Intrinsic pathway

Extrinsic pathway

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27
Q

What does the intrinsic pathway involve

A

1) genotoxic damage is detected
2) cytochrome c is released from the mitochondria
3) cytochrome c binds to a path 1 activator
4) caspase 9 is activated with results in apoptosis

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28
Q

What does the extrinsic pathway involve

A

1) pathway relies on tumour necrosis family receptor (TNFR)

2) TNFR activates caspase that initiates apoptosis

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29
Q

Which pathway does agents select for apoptosis

A

Different agents select different pathways either intrinsic or extrinsic

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30
Q

What protein does some cancer release that increases the threshold for apoptosis

A

BCL-2

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31
Q

What has to happen for the intrinsic pathway to become activated

A

DNA damage from chemotherapy

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32
Q

What detects the cellular stress in the intrinsic pathway to activate it

A

P53 detect DNA damage and activates the intrinsic pathway

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33
Q

What determines the activation of the extrinsic pathjwaty

A

Condition in the extracellular environment

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34
Q

What phase of the cycle does anti-metabolites work at

A

DNA synthesis (s phase)

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35
Q

Give an example of a anti-metabolite drug

A

5-flurouracil

36
Q

What structure does 5-flurouracil have

A

Pyramidine with flurocine attached to it

37
Q

In a normal cell how are nucleotides metabolised e.g thymidine

A

1) DUMP acquire methyl group via thymidine synthetase and folic acid to become DTMP
2) DTMP becomes phosphorylated into DTDP
3) DTDP becomes phosphorylated into DTTP i.e thymidine
4) thymidine becomes incorporated into DNA during DNA synthesis

38
Q

How does 5fluro-uracil act

A

1) 5FU becomes incorporated to DUMP to from to Fluorodeoxyuridine monophosphate (FDUMP)
2) FDUMP inhibits thymidine synthetase
3) thymidine cannot be produced and DNA synthesis cannot occur
4) apoptosis occurs

39
Q

What are the actions of anthracyclines

A
  • inhibit topoisomerase 2
  • induce free radical formation that bind to dna
  • DNA intercalaton for DS or SSDNA break
40
Q

Name an example of topoisomerase 2 inhibitor

A

Anthracycline

41
Q

Name examples of anthracycline drugs

A

Doxorubicin

42
Q

By blocking topo-isomerase what does it prevent

A

Uncoiling of DNA to stop replication and gene expression

43
Q

How do athracycline block the action of topoisomerase 2

A

By binding to the enzyme topoisomerase 2

44
Q

What are the 2 forms of topoisomerase inhibitors

A

Topoisomerase 1

Topoisomerase 2

45
Q

What is the monomeric form

A

ATP independent

46
Q

What is the normal action of topoisomerase 1

A

Cleave one strand of the dna

47
Q

Name examples of topoisomerase 1 inhibitor

A

Anthracylcines

Camptothecin analogues

48
Q

What are dimer forms

A

Atp dependent

49
Q

What is the normal action of topoisomerase 2

A

Bind to double stranded dna to cleave both strands

50
Q

Name examples of topoisomerase 2 inhibitors

A

Anthracycline

Epipodophylotoxins

51
Q

What does anthracylines have

52
Q

What can toxicity of anthracylines cause

A 
Myelosupression 
GIT
Local tissue damage 
Alopecia 
Cardio toxicity
53
Q

What do microtubules form

A

Cytoskeleton of cells

54
Q

What are microtubules involved in

A 
Mitotic spindles 
Chemotaxis 
Membrane scaffolding 
Intracellular transport 
Signalling
55
Q

When microtubules inhibitors inhibit microtubules what does it impair

A

The normal functions of microtubules

56
Q

What are the 2 groups of microtubules inhibitors

A

Vinca alkaloids

Taxanes

57
Q

How do vinca alkaloids functions

A

Stop assembly and dissembley of microtubules i.e stop the production/formation of new microtubules (destabilises)

58
Q

What cell cycle phase does vinca alkaloids work in

A

M phase (arrest it)

59
Q

What toxicity does vinca alkaloids show

A

Neurones
GI
Marrow

60
Q

How do taxanes function

A

Stabilise microtubules and inhibit dynamic reorganisation i.e break microtubules that have already formed (stabilises)

61
Q

At what cell cycle phase does taxanaes work at

A

Anaphase and metaphase

62
Q

What toxicity does taxanes show

A

Neurones

Marrow

63
Q

How do alkaylting agents work

A

Bind to guanine crosslink DNA strands

63
Q

When alkylating agents bind to DNA what do they affect

A

DNA translation and transcription

64
Q

Name another group of drugs that are similar to alkalyting agents

A

Platinum analogues

65
Q

How does platinum analogues function

A

Charged particle binds convently to macromolecules e.g dna

67
Q

What does platinum analogues form

A

Intra stand DNA adducts

68
Q

Name an example of a platinum analogue

A

Cis platin

69
Q

What do some chemotherapy agents cause the release of to signal an eat me signal to the immune system so the cell is engulfed

A

Calreticulin

70
Q

During apoptosis what can chemotherapy agents cause the releases of so dendritic cells are attracted to the site and makes the tumour to become engulfed

71
Q

During secondary necrosis what can chemotherapy agents cause the release of

72
Q

What does HMBG1 cause

A

Attraction of dendritic cells to the tumour

73
Q

Therefore apart from killing the cells what other role does chemotherapy agent shave

A

Exposing the cells to the immune system for further killing of cells

74
Q

What are the 4 clinical uses of chemotherapy

A

Primary chemotherapy
Neo-adjuvant
Adjuvant
Chemoradiotherapy

75
Q

What is primary chemotherapy

A

The main treatment of cancer so the tumour shrinks and goes away

76
Q

What is neo adjuvant chemotherapy

A

To reduce the size of the tumour before surgery

77
Q

What is adjuvant chemotherapy

A

Chemotherapy that is used after the surgery to remove microscopic tumour and prevent relapse of cancer

78
Q

What is chemo radiotherapy

A

Ionizing therapy is the primary treatment but giving additional cytotoxic chemotherapy makes it sensitiser for radiation

79
Q

What does chemotherapy target

A

Dividing cells

80
Q

Can a proportion of tumour cells be non diving cells

81
Q

Is a proportion of tumour cells are non dividing what happens to the susceptibility of the cell to chemotherapy

82
Q

What happens to the cells in cell division as the tumour size increases

83
Q

What other feature does large tumour have that make is less resistant to chemotherapy

A

Drug resistant clones

84
Q

Therefore overall why are large tumours resistant to chemotherapy

A

They have resistant clones

They have more cells that are non dividing

85
Q

To kill cancer cells as much as possible what do we need the doses of cytotoxic drugs

A

Close to tolerated dose

86
Q

To squeeze cycles together what agent can we use in chemotherapy

87
Q

What does GSF do

A

Increase neutrophil recovery rate between the cycles of chemotherapy and the bone marrow recovers faster

CAN (25 decks)

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