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PMCOL 200 > Chemotherapy > Flashcards

Chemotherapy Flashcards

(76 cards)

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1
Q

What is the leading cause of death in Canada?

A

Cancer (1/4)

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2
Q

Approx. how many types of cancer are there?

A

Over 100

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3
Q

What is cancer?

A

Abnormal cell growth w/ potential to spread to other parts of body (metastasis)

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4
Q

What are 4 environmental factors assoc w/ cancer? And genetic factor?

A

Tobacco, ionizing radiation, enviro pollution (asbestos, radon), viral infections (HIV, HPV); BRCA 1 in breast cancer (incr risk of getting cancer vs wo/ gene)

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5
Q

What fundamentally causes cancer?

A

Mutations in genes that regulate cell growth

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6
Q

What are the 4 phases of and their purpose in the cell cycle? Extra phase?

A

G1: checkpoint to ensure cell is ready for DNA synth (40%)
S: DNA synth (39%)
G2: checkpoint to ensure cell is ready for mitosis(19%)
M: mitosis (2%)
G0: quiescent state

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7
Q

What are the 2 types of genes important for regulation of the cell cycle?

A

Tumour suppressor genes and oncogenes

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8
Q

What are tumour suppression genes?

A

Repress cell cycle or promote apoptosis when mutation is detected

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9
Q

What 3 ways can tumour suppressor genes inhibit cell cycle/promote apoptosis?

A
  1. Inhibit cell cycle
  2. Initiate apoptosis after permanent DNA damage
  3. DNA repair proteins (BRCA)
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10
Q

What is p53?

A

Tumour suppressor protein that regulates cell cycle (mutated in 50% of tumours)

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11
Q

What are proto-oncogenes?

A

Normal genes involved in cell growth/proliferation and inhibition of apoptosis

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12
Q

What can cause proto-oncogenes to become oncogenes (incr expression)?

A

Mutations

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13
Q

What 2 mutations can convert proto-oncogenes to oncogenes?

A

Point mutations: small scale index’s that affect its expression
Chromosomal translocation: 2 separate chromosomal regions become abnormally fused

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14
Q

What is the Philadelphia chr? What is it an ex of?

A

Specific genetic abnormality in chr 22 (fused w/ chr 9) found in leukaemia cancer cells; chromosomal translocation

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15
Q

What causes the mutated chr 22 in Philadelphia chr? And result?

A

Region on chr 9 that encodes gene ABL is susceptible to breakage and combines w/ broken region on chr 22 that encodes for gene BCR creating BCR-ABL gene

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16
Q

What does the BCR-ABL gene cause?

A

Unregulated expression of tyrosine kinase activity leading to unregulated cell cycle/division

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17
Q

T/f: usually >1 oncogenes and tumour suppressor genes are mutated to cause cancer

A

True, can occur sequentially

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18
Q

1/3 of cancer patients are treated how?

A

Local treatment strategies (surgery or radiotherapy)

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19
Q

How are other cancer cases treated (not surgery/radiotherapy)? When are they used?

A

Systemic approaches w/ anti-cancer drugs; metastasis

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20
Q

What % of cancer patients can be cured w/ anti-cancer drugs when diagnosed at advanced stages?

A

10% (incr w/ combo of surgery and radiation)

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21
Q

what do anti-cancer drugs do?

A

Interfere w/ cell cycle (can target specific phases or be cytotoxic at all phases)

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22
Q

What makes tumour cells more susceptible to anti-cancer drugs that target S and M phases?

A

Tumour cells usually have more proliferating cells vs normal

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23
Q

What 3 normal tissues that proliferate rapidly are susceptible to damage from cytotoxic drugs?

A

Bone marrow, hair follicles, intestinal epithelium

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24
Q

T/f: most medications have a narrower TI and incr potential for harmful effects that anti-cancer drugs

A

False, anti-cancer drugs have a very narrow TI and high potential for severe side effects

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25
What are 3 types of anti-cancer drugs?
DNA synthesis inhibitors, natural products, miscellaneous
26
What are 4 ex of DNA synthesis inhibitors?
Pyrimidine analogues, purine analogues, alkylation agents, anti-folates
27
What are the 2 purine vs 2 pyrimidines in DNA and RNA replacement?
Purines: adenine and guanine Pyrimidines: cytosine and thymine (uracil in RNA)
28
What do pyrimidine analogues compete for?
Thymidylate synthase (TS) enzymes w/ normal pyrimidine precursors
29
What conversion does TS coordinate?
dUMP (deoxy-uracil monophos) to dTMP (deoxy-thymine monophos) via methylation
30
What is an ex of a pyrimidine analogue?
5-fluorouracil (5-FU)
31
What is the active metabolite of 5-FU (inactive)?
FdUMP
32
What do purine analogues inhibit?
phosphoribosyl pyrophosphate amidotransferase (PRPP amidotransferase) enzyme that synthesizes NT
33
What is an ex of a purine analogue?
6-mercaptopurine
34
t/f: PRPP amidotransferase is the rate-limiting factor for purine synthesis
true (alters synth/func'n of RNA and DNA)
35
what are alkylating agents?
highly reactive compounds that covalently bind to chemical groups in NTs causing cross-links and strand breakage
36
what atom is particularly susceptible to formation of covalent bonds w/ alkylating agents?
N7 atom of guanine (N on small ring by =O)
37
at what stage(s) in the cell cycle are cancer cells most susceptible to alkylating agents?
late G1 and S phase (DNA repl'n)
38
what is cisplatin?
platinum analogue that is an alkylating agent (inhibit DNA synth and func'n)
39
what are anti-folates?
folic acid analogues that interfere w/ FH4 metabolism and inhibit DNA repl'n
40
what is folic acid? what is it converted to?
essential dietary factor: FH4 cofactors
41
how are FH4 cofactors involved in DNA synthesis?
provide methyl groups for synthesis of DNA and RNA precursors (thymine or uracil)
42
what is methotrexate?
folic acid analogue that binds w/ high affinity to dihydrofolate reductase (enzyme that metabolizes folic acid)
43
when are anti-folates (methotrexate) most effective in the cell cycle?
S phase when cell are rapidly proliferating
44
what are natural products for cancer?
compounds extracted from plants/bacteria w/ anti-cancer properties
45
what are 4 ex of natural anti-cancer products?
vinca alkaloids, taxanes, epipodophyllotoxins, camptothecins
46
what are vinca alkaloids derived from?
periwinkle plant (Vinca rosea)
47
what do vinca alkaloids do?
inhibit tubulin polymerization
48
how do vinca alkaloids preventing tubulin polymerization treat cancer cells?
disrupts microtubule assembly in M phase for the mitotic spindle apparatus
49
what are taxanes derived from?
pacific yew tree (Taxus brevifolia)
50
what do taxanes do?
inhibit MT depolymerization (promote assembly) through high-affinity binding
51
how do taxanes promoting MT assembly/inhibiting depolymerization treat cancer cells?
inhibits mitosis and cell division (M phase)
52
what is an ex of a taxane?
paclitaxel
53
what are camptothecins derived from?
camptotheca acuminata tree
54
what are DNA topoisomerases? what do they do?
nuclear enzymes that reduce DNA supercoiling during DNA synthesis through single-strand breaks and resealing
55
how do camptothecins affect topoisomerases? and thus DNA synthesis?
bind and stabilize DNA-topoisomerase complex 1 which inhibits re-ligation step; accumulates single-strand break in DNA
56
what phase in the cell cycle are camptothecins specific for? why?
S-phase; require ongoing DNA synthesis for cytotoxicity
57
how do products of the soil microbe Streptomyces exhibit anti-cancer action? (anti-biotic)
intercalate DNA which blocks DNA synthesis and cell replication
58
what are anthracyclines (doxorubicin)?
anti-biotics that are the most widely used anti-cancer drugs
59
what are the 4 mechanisms of action of anthracyclines (doxorubicin)?
1. inhibit topoisomerases (~camptothecins) 2. generate free radicals (DNA mutagenesis->apoptosis) 3. bind to DNA w/ high affinity (affect synthesis/repl'n) 4. bind to pmemb and alters fluidity and ion transport
60
how do tyrosine kinase inhibitors treat cancer?
inhibit tyrosine kinase domain of Bcr-Abl oncoprotein (Philadelphia chr) to control unreg cell division
61
what form of cancer do tyrosine kinase inhibitors treat?
leukemia
62
what is an ex of tyrosine kinase inhibitors?
imantinib
63
t/f: epidermal growth factor receptors (EGFR) are over-expressed in a number of solid tumours
true
64
what does activation of EGFRs cause? (4)
promotion of cell growth/proliferation, invasion, metastasis, and angiogenesis
65
what is cetuximab?
monoclonal antibody that acts as an EGFR inhibitor
66
what is an ex of a hormonal anti-cancer agent?
tamoxifen
67
what is tamoxifen? what does it do?
selective estrogen receptor antagonist; blocks binding of estrogen to estrogen-sensitive cancer cells in breast tissue (breast cancer)
68
how can estrogen cause breast cancer?
cause cell growth/proliferation in breast tissue
69
what are 3 adverse effects of anti-cancers?
drug resistance, adverse symptoms in rapidly growing tissues, secondary malignancies
70
what are 2 kinds of drug resistance? diff?
primary: spontaneous wo/ exposure to drug (p53 mutations) acquired: response to anticancer
71
how can cancerous cells achieve resistance?
are rapidly dividing therefore have greater possibility for acquiring mutations that confer resistance
72
t/f: adverse symptoms to anti-cancers are not dose-related
false, are dose-related
73
what 3 rapidly growing tissues can show adverse effects to anti-cancers?
bone marrow, intestinal mucosa, and reproductive system
74
what are 5 adverse symptoms of anti-cancers?
impaired immune system, diarrhea, hair loss, nausea, and vomiting
75
what are secondary malignancies?
cancer that is associated w/ anticancer drugs
76
what is an ex of how anti-cancers can be carcinogenic in nature?
anti-biotics incr mutations (in cancer cells) but can backfire if it occurs in previously unaffected cells

PMCOL 200 (27 decks)

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