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PMCOL 200 > Chemotherapy > Flashcards

Chemotherapy Flashcards

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
Q

What are 3 types of anti-cancer drugs?

A

DNA synthesis inhibitors, natural products, miscellaneous

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26
Q

What are 4 ex of DNA synthesis inhibitors?

A

Pyrimidine analogues, purine analogues, alkylation agents, anti-folates

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27
Q

What are the 2 purine vs 2 pyrimidines in DNA and RNA replacement?

A

Purines: adenine and guanine
Pyrimidines: cytosine and thymine (uracil in RNA)

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28
Q

What do pyrimidine analogues compete for?

A

Thymidylate synthase (TS) enzymes w/ normal pyrimidine precursors

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29
Q

What conversion does TS coordinate?

A

dUMP (deoxy-uracil monophos) to dTMP (deoxy-thymine monophos) via methylation

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30
Q

What is an ex of a pyrimidine analogue?

A

5-fluorouracil (5-FU)

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31
Q

What is the active metabolite of 5-FU (inactive)?

A

FdUMP

32
Q

What do purine analogues inhibit?

A

phosphoribosyl pyrophosphate amidotransferase (PRPP amidotransferase) enzyme that synthesizes NT

33
Q

What is an ex of a purine analogue?

A

6-mercaptopurine

34
Q

t/f: PRPP amidotransferase is the rate-limiting factor for purine synthesis

A

true (alters synth/func’n of RNA and DNA)

35
Q

what are alkylating agents?

A

highly reactive compounds that covalently bind to chemical groups in NTs causing cross-links and strand breakage

36
Q

what atom is particularly susceptible to formation of covalent bonds w/ alkylating agents?

A

N7 atom of guanine (N on small ring by =O)

37
Q

at what stage(s) in the cell cycle are cancer cells most susceptible to alkylating agents?

A

late G1 and S phase (DNA repl’n)

38
Q

what is cisplatin?

A

platinum analogue that is an alkylating agent (inhibit DNA synth and func’n)

39
Q

what are anti-folates?

A

folic acid analogues that interfere w/ FH4 metabolism and inhibit DNA repl’n

40
Q

what is folic acid? what is it converted to?

A

essential dietary factor: FH4 cofactors

41
Q

how are FH4 cofactors involved in DNA synthesis?

A

provide methyl groups for synthesis of DNA and RNA precursors (thymine or uracil)

42
Q

what is methotrexate?

A

folic acid analogue that binds w/ high affinity to dihydrofolate reductase (enzyme that metabolizes folic acid)

43
Q

when are anti-folates (methotrexate) most effective in the cell cycle?

A

S phase when cell are rapidly proliferating

44
Q

what are natural products for cancer?

A

compounds extracted from plants/bacteria w/ anti-cancer properties

45
Q

what are 4 ex of natural anti-cancer products?

A

vinca alkaloids, taxanes, epipodophyllotoxins, camptothecins

46
Q

what are vinca alkaloids derived from?

A

periwinkle plant (Vinca rosea)

47
Q

what do vinca alkaloids do?

A

inhibit tubulin polymerization

48
Q

how do vinca alkaloids preventing tubulin polymerization treat cancer cells?

A

disrupts microtubule assembly in M phase for the mitotic spindle apparatus

49
Q

what are taxanes derived from?

A

pacific yew tree (Taxus brevifolia)

50
Q

what do taxanes do?

A

inhibit MT depolymerization (promote assembly) through high-affinity binding

51
Q

how do taxanes promoting MT assembly/inhibiting depolymerization treat cancer cells?

A

inhibits mitosis and cell division (M phase)

52
Q

what is an ex of a taxane?

A

paclitaxel

53
Q

what are camptothecins derived from?

A

camptotheca acuminata tree

54
Q

what are DNA topoisomerases? what do they do?

A

nuclear enzymes that reduce DNA supercoiling during DNA synthesis through single-strand breaks and resealing

55
Q

how do camptothecins affect topoisomerases? and thus DNA synthesis?

A

bind and stabilize DNA-topoisomerase complex 1 which inhibits re-ligation step; accumulates single-strand break in DNA

56
Q

what phase in the cell cycle are camptothecins specific for? why?

A

S-phase; require ongoing DNA synthesis for cytotoxicity

57
Q

how do products of the soil microbe Streptomyces exhibit anti-cancer action? (anti-biotic)

A

intercalate DNA which blocks DNA synthesis and cell replication

58
Q

what are anthracyclines (doxorubicin)?

A

anti-biotics that are the most widely used anti-cancer drugs

59
Q

what are the 4 mechanisms of action of anthracyclines (doxorubicin)?

A
  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
Q

how do tyrosine kinase inhibitors treat cancer?

A

inhibit tyrosine kinase domain of Bcr-Abl oncoprotein (Philadelphia chr) to control unreg cell division

61
Q

what form of cancer do tyrosine kinase inhibitors treat?

A

leukemia

62
Q

what is an ex of tyrosine kinase inhibitors?

A

imantinib

63
Q

t/f: epidermal growth factor receptors (EGFR) are over-expressed in a number of solid tumours

A

true

64
Q

what does activation of EGFRs cause? (4)

A

promotion of cell growth/proliferation, invasion, metastasis, and angiogenesis

65
Q

what is cetuximab?

A

monoclonal antibody that acts as an EGFR inhibitor

66
Q

what is an ex of a hormonal anti-cancer agent?

A

tamoxifen

67
Q

what is tamoxifen? what does it do?

A

selective estrogen receptor antagonist; blocks binding of estrogen to estrogen-sensitive cancer cells in breast tissue (breast cancer)

68
Q

how can estrogen cause breast cancer?

A

cause cell growth/proliferation in breast tissue

69
Q

what are 3 adverse effects of anti-cancers?

A

drug resistance, adverse symptoms in rapidly growing tissues, secondary malignancies

70
Q

what are 2 kinds of drug resistance? diff?

A

primary: spontaneous wo/ exposure to drug (p53 mutations)
acquired: response to anticancer

71
Q

how can cancerous cells achieve resistance?

A

are rapidly dividing therefore have greater possibility for acquiring mutations that confer resistance

72
Q

t/f: adverse symptoms to anti-cancers are not dose-related

A

false, are dose-related

73
Q

what 3 rapidly growing tissues can show adverse effects to anti-cancers?

A

bone marrow, intestinal mucosa, and reproductive system

74
Q

what are 5 adverse symptoms of anti-cancers?

A

impaired immune system, diarrhea, hair loss, nausea, and vomiting

75
Q

what are secondary malignancies?

A

cancer that is associated w/ anticancer drugs

76
Q

what is an ex of how anti-cancers can be carcinogenic in nature?

A

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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