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.Pharmacology > Part 7: Cancer Treatments 1 > Flashcards

Part 7: Cancer Treatments 1 Flashcards

1
Q

define cancer

A

disease characterized by a defect in normal control mechanisms that govern cell survival, proliferation and differentiation

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2
Q

loss of ___ allows tumors to grow excessively and disrupt normal physiologic functions or organs and tissues

A

regulatory components

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3
Q

what are some cancer risks we cannot control?

A

age, sex, race, genetics

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4
Q

which sex is at higher risk of cancer

A

men, but women are close approaching

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5
Q

does the presence of certain genes or biomarkers that are linked to cancer mean that you will definitely develop cancer?

A

no

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6
Q

what are the most important determinants of cancer development?

A

environmental factors

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7
Q

what are the environmental factors that affect cancer development?

A

UV and radiation exposure, chemicals iin smoking tobacco

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8
Q

what virus has been shown to increase the risk of cervical cancer for women?

A

HPV

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9
Q

t/f lifesytle conditions like diet and exercise influence cancer risk

A

t

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10
Q

t/f cancer is the leading cause of death in canada

A

t

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11
Q

what are the 4 most common cancers in Canada?

A
  1. lung cancer
  2. breast cancer
  3. colorectal cancer
  4. Prostate cancer
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12
Q

t/f survival rates of cancer are increasing

A

t

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13
Q

t/f tumour cells originate from normal cells

A

t

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14
Q

how does cancer growth start?

A

chemical or physical carcinogen causes mutation

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15
Q

what happens in the “promotion” stage of cancer development?

A

cell division promoted by promoting and growth factors

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16
Q

t/f cancer initiators can also be promotors

A

t

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17
Q

an example of an initiator that can also be a promotor

A

cigarette smoke

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18
Q

do all cell mutations go on to daughter cells? why or why not?

A

no; because sometimes the cells can fix the mistake before or die before reproducing

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19
Q

t/f there can be multiple mutations within a population of cells

A

t

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20
Q

what happens in the “progression” stage of cancer development?

A

transformation to malignancy, further mutation and variability in the tumour

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21
Q

what does it mean when a tumour becomes malignant?

A

tumour has transformed so that its cellular process are no longer tightly controlled and regulated like normal cells

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22
Q

a hallmark of tumour biology is that the cells become invasive and take over ___

A

neighbouring tissues

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23
Q

what is stage 0 cancer?

A

early cancer, not detectable, stays at site of origin (in situ)

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24
Q

what are stages 1-3 cancer?

A

tumour is increasing in size and spread

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25
Q

what is stage 4 cancer?

A

tumour has invaded into other tissues and there is metastasis

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26
Q

what is contact inhibition?

A

in normal cells, when they come in contact with a neighbouring cell, they stop growing

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27
Q

do cancer cells have contact inhibitions?

A

no

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28
Q

as a tumour gets larger, it requires additional nutrinets to feed its growth, so it recruits ___ and ___. to meet its metabolic needs

A

blood vessels and lymph nodes

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29
Q

at what stages are tumours typically detected?

A

2-3

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30
Q

why are tumours typically detected at stages 2-3?

A

onset of symptoms

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31
Q

in colon cancer, the invasion of the tumour across the colon membrane is likely to cause what detectable symptom?

A

blood in the stool

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32
Q

in what stage does a tumour have a rich blood and lymph supply?

A

stage 4

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33
Q

what are the common sites of secondary tumours that come off a stage 4 tumour?

A

areas that are highly perfused (liver, brain, lungs)

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34
Q

what are the 3 main ways to treat cancer?

A
  1. surgical removal
  2. radiation
  3. chemotherapy
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35
Q

radiation is very effective at killing cancer cells, so why is it limited?

A

limited to cells near the surface of the skin (skin, head and neck cancers_

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36
Q

does radiation specifically target cancer cells ?

A

no

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37
Q

chemotherapy is also called ____ (3)

A
  1. antineoplastic drugs
  2. anticancer drug
  3. immunotherapy
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38
Q

what are antineoplastic drugs?

A

drugs that prevent the growth of abnormal cells (neoplasms)

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39
Q

how do antineoplatic drugs work to prevent abnormal cell grwth?

A

interfering with aspects of the cell cycle and preventing rapidly dividing cells from proliferating

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40
Q

there are some newer drugs that target tumour ___ or ____ that have been shown to be increased in cancer cells

A

biomarkers and cellular processes

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41
Q

what is the aim of immuotherapy in cancer treatment?

A

to enhance the responsiveness of the host immune system to be able to recognize tumour cells and remove them

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42
Q

why is it such a challenge to only target cancer cells in chemo?

A

tumour cells originate from host cells, so they have all the same cellular parts as our normal cells

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43
Q

what is a typical target of antineoplastic drugs?

A

quickly dividing cells

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44
Q

does the approach to target “rapidly dividing cells” spare all healthy cells?

A

no

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45
Q

t/f the max tolerable dose of anti-cancer medications should be used

A

true

46
Q

t/f the chosen cancer treatment must be tolerable so the whole course of treatment can be completed

A

t

47
Q

why is it typical to give multiple anti-cancer agents with different MOAs?

A

used to increase tumour killing rate; reduce resistance and facilitate low dose to protect against ADRs

48
Q

why is chemo typically given in cyclic rounds?

A

reduce ADR by allowing healthy tissues to repair themselves

49
Q

many tumours are apprximated to follow a ____ growth pattern

A

exponential

50
Q

what is the typical size of a tumour that can be detected?

A

1cm3, small green pea

51
Q

what is reccurence of cancer?

A

after removal of cancer, some cells remain and start to grow new tumours

52
Q

if chemo treatments are spaced too far apart, what can happen?

A

cancer cell #s increase too much

53
Q

what are the 2 key processes of the cell cycle that allow proliferation of tumour cells?

A
  1. S phase (making copy of DNA

2. M phase (mitosis)

54
Q

what is the prototypic example of an alkylating agent?

A

cyclophosphamide

55
Q

what is the MOA of cyclophosphamide?

A

have reactive chemical groups that bind covalently toDNA causing disruption to shape of the alpha helix and cause the strand to break

56
Q

if damaged DNA cannot be repaired, it triggers ___

A

cell death

57
Q

t/f normal cells may be better at repairing damaged DNA than cancer cells

A

t

58
Q

alkylating agents, like cyclophosphamide bind ____ (reversibly/irreversibly) to DNA

A

irreversibly

59
Q

what are topoisomerases?

A

enzymes that unwind DNA strands that allow transcription to proceed smoothly

60
Q

what do topoisomerase enzymes do?

A

introduce temporary strand breaks in the DNA strands to prevent tangling and supercoiling

61
Q

what happens to the breaks caused by topoisomerases?

A

quicly repaired to maintain the structural integrity of th eDNA

62
Q

what do topoisomerase inhibitors do?

A

stall the uncoiling process and halt DNA replication

63
Q

____ is an example of an antibiotic isolated from bacteria that has anti-cancer activity

A

doxorubicin

64
Q

what is doxorubicin?

A

natural product isolated from Step. speciies

65
Q

doxorubicin is a ____ type antibiotic

A

anthracycline

66
Q

anthracycline antibiotics like doxorubicin hava a unique ____- that gives them several cytotoxic effects

A

chemical structure

67
Q

the ____ structure of the doxorubicin molecule wedges between the DNA strands and pushes them apart

A

flat ring structure

68
Q

what happens if toposoimerase comes along to a strand of DNA that has been impacted by doxorubicin?

A

forma a static complex with the DNA molecule and the drug and prevents the progression of DNA replication, triggers cell death

69
Q

doxorubicin forms ____ by its O2 containing groups

A

free radicals

70
Q

what is the significance of doxorubicin forming free radicals?

A

causes additional DNA damage and cellular toxicity, causing death

71
Q

what is a common ADR of doxorubicin that can limit its use?

A

cardiac toxicity

72
Q

t/f it is not entirely clear of doxorubicin is more toxic to cardio cells compared to other cells

A

t

73
Q

in order to make new DNA, cells must make more ____, the building blocks of DNA and RNA

A

nucleotides

74
Q

___ and ___ precursors, using importnat components like ___ are assembled into nucleotides to be ready for incorporation into newly made DNA strands

A

purine and pyrimidine ; folate

75
Q

____ are a subclass of antineoplastic drugs that interfere with the biosynthesis of nucleotides

A

antimetabolites

76
Q

if DNA synthesis is halted due to the lack of available nucleotides, _____ pathways are initiated

A

cell death

77
Q

when antimetabolites interfere with nucleotide synthesis, modified DNA and RNA may be made, but they wont make the proper ___

A

structures

78
Q

dive an example of an antimetabolite used for cancer

A

methotrexate

79
Q

methotrexate is structurally similar to ___

A

folate

80
Q

methotrexate interacts with the ___ enzyme

A

dihydrofolate reductase

81
Q

what is the function of methotrexate?

A

inhibits dihydrofolate reductase, reducing nucleotide and DNA synthesis

82
Q

at low doses, methotrexate can be used for inflammatory conditions such as ___ to slow the proliferation of ____ cells

A

rheumatoid arthritis; immune

83
Q

at higher doses, methotrexate reduces the proliferation of ____ cells

A

tumour

84
Q

5-fluorouracil is an example of a _____ type drug

A

antimetabolite

85
Q

the structure of 5-fluorouracil is structurally similar to ____ and ____ nucleotide bases

A

uracil and thiamine

86
Q

5-flouraouracil’s structure allows it to be ____ withinthe cell

A

metabolized

87
Q

the 5-flourouracil metabolite, _____, inhibits thymidylate synthase, a critcal enzyme in the making of nucleotides

A

FdUMP

88
Q

5-FU binds to ____, preventing further synthesis of thymidine nucleotides

A

thymidylate synthase

89
Q

5-FU binds to TS ____ (irreversibly/reversibly)

A

irreversibly

90
Q

what is the significance of 5-FU binding to TS?

A

prevents DNA from being made, starting cell death pathways

91
Q

t/f antimetabolites interfere with the making of DNA precursors by having structural similarities with the endogenous substrates of the pathway

A

t

92
Q

microtubules are critical structural components of ____

A

mitosis

93
Q

what is the role of microtubles?

A

forming the mitotic spindles that organize the newly duplicated chromosomes and pull individual cells apart tp make daughter cells

94
Q

microtubules consist of many ____ that dynamically assemble and disassemble to achieve the desired actions

A

tubulin dimers

95
Q

interfering with the dynamic nature of microtubles can prevent ____

A

cellular division

96
Q

what is vincristine?

A

a vinca alkaloid (another class of natural product compounds isolated from plants)

97
Q

MOA of vincristine

A

prevents microtubule assembly and breaking down tubulin dimers, thus stopping cancer mitosis

98
Q

what are taxanes?

A

class of antimicrotubule agents originally isolated from plants

99
Q

give an example of a taxane

A

paciltaxel (taxol)

100
Q

MOA of taxanes

A

prevents disassembly of microtubules, tubulin dimers still assemble, but there is no dynamic acticvity bc the disassembly is blocked

101
Q

t/f the outcomes of vincristine and paclitaxela are the same, but the mechanisms are opposite

A

t

102
Q

an ADR with antimicrotubule agents, especially with vincristine is the development of ____

A

neuropathies

103
Q

what do antimicrotubules cause neuropathies?

A

due to impairing the important functions of microtubules in neurons

104
Q

antimicrotubule agents are ___phase agents

A

M

105
Q

antimetabolites are ___ phase agents

A

S

106
Q

agents that act only during specific periods of cell cycle may be more effective in tumours that are ___ growing and less so in tumours that are ___ growing

A

fast; slow

107
Q

t/f drugs like cyclophosphamide bind to DNA at any time and cause damage regardless of cell phase

A

t

108
Q

cyclophosphamide and doxorubicin are classed as a ____agent

A

non-cell sycle specific

109
Q

t/f oral mucositis is a common ADR of chemo

A

t

110
Q

why does chemo lead to oral mucositis?

A

breakdown of protective barrier opens the door to infections (many concer pts are immunocomprosmised already)

111
Q

what ca be used for oral mucositis?

A

oral rinses, topical anesthetics, saliva replaemnets, antibiotics

.Pharmacology (55 decks)

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