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Pharm > Lecture 26: Cancer Chemotherapy > Flashcards

Lecture 26: Cancer Chemotherapy Flashcards

1
Q

What is the leading cause of death in Canada?

A

Cancer

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2
Q

What is cancer characterized by?

A

Abnormal cell growth with potential to spread to other parts of the body (metastasis)

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3
Q

What is Cancer caused by?

A

Environmental and genetic factors

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4
Q

What is Radon?

A

A naturally occuring gas that occurs in the environment the causes lung cancer

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5
Q

How can cancer be associated with viral infections?

A
  • HIV with hodgkin’s and non-hodgkin’s lymphoma

* HPV with cervical cancer

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6
Q

What are the characteristics of genes associated with cancer?

A

They are low penetrating genes, meaning the mutations only slightly increase risk but not substantially. But some are high penetrance like BRCA 1

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7
Q

When does cancer arise?

A

When genes that regulate cell growth are mutated

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8
Q

What happens in a normal cell if there is a mistake in duplicating the genetic material?

A

Either its fixed or the cell undergoes apoptosis

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9
Q

What are the 5 phases in the cell cycle?

A
  1. GI phase
  2. S phase
  3. G2 phase
  4. M phase
  5. G0 phase
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10
Q

What is the GI phase?

A

A checkpoint to ensure cell ready for DNA synthesis

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11
Q

What is the S phase?

A

DNA synthesis

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12
Q

What is the G2 phase?

A

Checkpoint to ensure cell is ready for mitosis

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13
Q

What is the M phase?

A

Mitotic phase (cell divided)

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14
Q

What is the G0 phase?

A

The Quiescent state

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15
Q

What are the two groups of genes important in the regulation of the cell cycle?

A
  • Tumor suppressor genes

* Oncogenes

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16
Q

What is the longest part of the cell cycle?

A

G1

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17
Q

What is the shortest part of the cell cycle?

A

M

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18
Q

What do Tumor suppressor genes do?

A

Repress the cell cycle or promote apoptosis

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19
Q

What three ways do tumor suppressor gene repress the cell cycle or promote apoptosis?

A
  1. Inhibit cell division
  2. Initiate apoptosis following irreversible DNA damage
  3. DNA repair proteins (BRCA) can repair
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20
Q

What happens if there is a mutation in the tumor suppressor genes?

A

Then they cannot suppress cell division

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21
Q

What is p53?

A

A tumor suppressor protein that regulates the cell cycle

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22
Q

What are the characteristics of p53 in tumors?

A

It is mutated in 50% of all tumors

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23
Q

What are Proto-oncogenes?

A

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

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24
Q

What can mutations in oncogenes do?

A

Increase expression causing increase cell growth and proliferation

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25
Q

what are the two types of mutations?

A
  • Point mutations

* Chromosomal translocation

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26
Q

What are point mutations?

A

Small scale deletion or insertions which affect its expression

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27
Q

What is chromosomal translocation?

A

When two separate chromosomal regions become abnormally fused

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28
Q

What is Philadelphia chromosome?

A

A specific genetic abnormality in chromosome 22 found in leukemia cancer cells (abnormal translocation of chromosome 9 and 22)

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29
Q

What gene does the fusion in the Philadelphia chromosome create?

A

A new gene BCR-ABL

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30
Q

What does the BCR-ABL gene lead to?

A

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

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31
Q

What acts in concert to cause cancer?

A

Usually multiple oncogenes and mutated tumor suppressor genes

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32
Q

What is 1/3 of cancer treated with?

A

Local treatment strategies such as surgery or radiotherapy

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33
Q

What approach for cancer treatment is required when metastasis is present?

A

A systemic approach

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34
Q

What percentage of cancer drugs cure all cancer patients when the tumor is diagnosed at advanced stage?

A

10%

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35
Q

What do anti-cancer drugs do?

A

Interfere with cell cycle

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36
Q

When are anti-cancer drugs more effective?

A

When cancer is detected early or when used with other treatments

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37
Q

Which phases in the cell cycle do anti-cancer drugs usually work at?

A

The S and M phase

38
Q

Why are tumor cells more susceptible to S and M phase anti-cancer drugs?

A

Because they generally have a higher percentage of proliferating cells than normal cells

39
Q

What cells are susceptible to damage from cytotoxic drugs?

A

Normal tissues that proliferate rapidly (bone marrow, hair follicle, intestinal epithelium)

40
Q

What do Pyrimidine analogues do?

A

Compete with normal pyrimidine precursors for the enzyme thymidylate synthase (TS)

41
Q

What do Pyrimidine analogues compete with normal pyrimidines for?

A

The enzyme Thymidylate Synthase (TS)

42
Q

What is TS required for?

A

The conversion of dUMP to dTMP

43
Q

What kind of drug is 5-fluorouracil (5-FU)?

A

A pyrimidine analogue and a prodrug

44
Q

How does 5-FU work?

A

It looks like dUMP and competes for the active site of thymidylate synthase

45
Q

What is the active form of 5-FU?

A

FdUMP

46
Q

How is 5-FU activated?

A

In the liver with metabolism

47
Q

What kind of drug is 6-mercaptopurine?

A

A purine analogue

48
Q

How does 6-mercaptopurine work?

A

It inhibits purine nucleotide biosynthesis and metabolism by inhibiting an enzyme called PRPP amidotransferase

49
Q

What enzyme does 6-mercaptopurine inhibit?

A

PRPP amidotransferase

50
Q

What does PRPP amidotranferase do?

A

Takes the ribose sugar and converts it into an intermediate base pair called IMP that can be converted into GMP or AMP

51
Q

What is the rate limiting factor for purine synthesis?

A

The work of the enzyme PRPP amidotransferase

52
Q

What are Alkylating agents?

A

Highly reactive compounds which covalently link chemical groups found in nucleic acids

53
Q

What do Alkylating agents lead to?

A

Cross linking between strands of DNA and strand breakage

54
Q

What is particularly susceptible to the formation of covalent bonds with alkylating agents?

A

N7 atom of guanine

55
Q

When are cancer cells most susceptible to Alkylating Agents?

A

In the late G1 and S phases

56
Q

What drug is an Alkylating agent?

A

Cisplatin

57
Q

What kind of drug is Cisplatin?

A

An alkylating agent

58
Q

What is Folic acid converted into?

A

FH4 cofactors

59
Q

What do FH4 cofactors provide?

A

Methyl groups for the synthesis of precursors of DNA

60
Q

What do FH4 cofactors provide?

A

Methyl groups for the synthesis of precursors of DNA

61
Q

What do Folic Acid Analouges do?

A

Interfere with FH4 metabolism thereby inhibiting DNA replication

62
Q

What kind of drug is Methotrexate?

A

An anti-folate

63
Q

How does Methotrexate work?

A

Binds with high affinity to the active catalytic site of dihydrofolate reductase which inhibits production of FH4 cofactors

64
Q

During what stage of the cell cycle is Methotrexate effective?

A

During the S phase

65
Q

What drug is an anti-folate?

A

Methotrexate

66
Q

What are Natural Products?

A

Compounds extracted from plants or bacteria with anti-cancer properties

67
Q

What are the Natural Products?

A
  • Vinca Alkaloids
  • Taxanes
  • Epipodophyllotoxins
  • Camptothecins
68
Q

What are Vinca Alkaloids derived from?

A

The periwinkle plant

69
Q

What do Vinca Alkaloids do?

A

They inhibit tubulin polymerization which disrupts the assembly of microtubules involved in mitotic spindle apparatus (M phase)

70
Q

Which Phase do Vinca alkaloids act on?

A

The M phase

71
Q

What are Taxanes derived from?

A

The Pacific yew tree

72
Q

How do Taxanes work?

A

They promote microtubule assembly through high affinity binding which inhibits mitosis and cell division by preventing them from being dismantled

73
Q

Which phase do Taxanes work on?

A

The M phase

74
Q

What is an example of a Taxane?

A

Paclitaxel

75
Q

What kind of drug is Paclitaxel?

A

A taxane

76
Q

What are Camptothecins derived from?

A

Camptotheca acuminata

77
Q

What are DNA topoisomerases?

A

Nuclear enzymes that reduce torsional stress in supercoiled DNA through strand breakage and resealing

78
Q

What do Camptothecins do?

A

They bind and stabilize the normally transient DNA-topoisomerase I complex and inhibits the religation of DNA causing single stranded breaks in DNA

79
Q

What phase do Camptothecins affect?

A

The S-phase

80
Q

What is an antibiotic cancer drug?

A

Anthracycline

81
Q

What type of drug is Anthracycline?

A

An anti-cancer drug

82
Q

What are the four mechanisms of actions of Anthracycline?

A
  1. Inhibit topoisomerases
  2. Generate free radicals (DNA mutagenesis)
  3. High affinity binding to DNA
  4. Bind cellular membrane to alter fluidity and ion transport
83
Q

What do Tyrosine Kinase Inhibitors do?

A

Inhibit tyrosine kinase domain of the BCR-ABL oncoproteins

84
Q

What are Tyrosine Kinase inhibitors used to treat?

A

Leukemia

85
Q

How do Epidermal Growth factor inhibitors work?

A

They inhibit cell growth and proliferation

86
Q

What is Cetuximab?

A

A monoclonal antibody directed against the extracellular domain of EGFR

87
Q

What do Selective estrogen receptor antagonists do?

A

Blocks binding of estrogen to estrogen sensitive cancer cells in breast tissue

88
Q

What is a selective estrogen receptor antagonist?

A

Tamoxifen

89
Q

What is Primary resistance?

A

Spontaneous resistance in the absence of prior exposure to anti-cancer drugs so tumor was never susceptible to drugs

90
Q

What is acquired resistance?

A

Develops in response to anticancer drug

Pharm (31 decks)

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