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PMCOL 200 Final > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

What is metastasis?

A

abnormal cell growth with potential to spread to other parts of the body

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2
Q

What causes cancer?

A
  • environmental factors (e.g. tobacco, radiation, pollution)
  • viral infections (e.g. HIV)
  • genetics (e.g. BRCA1 in breast cancer)
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3
Q

What is cancer defined as, in terms of disease? Based on this definition, how does cancer arise?

A

cancer = disease of cell growth REGULATION

cancer arises when GENES that regulate cell growth are MUTATED

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4
Q

What occurs to a cancer cell when there is unfixable DNA damage?

a) apoptosis
b) cell continues dividing

A

b) cell continues dividing

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5
Q

What occurs to a normal cell when there is unfixable DNA damage?

a) apoptosis
b) cell continues dividing

A

a) apoptosis

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6
Q

What are all the phases of the cell cycle?

A

1) G1 phase: checkpoint to ensure cell is ready for DNA synthesis
2) S phase: DNA synthesis
3) G2 phase: checkpoint to ensure cell is ready for mitosis
4) M phase: mitotic phase (cell divides into 2 daughter cells)
5) G0 phase: quiescent state

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7
Q

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

A

1) tumor suppressor genes (and the proteins they encode)

2) oncogenes

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8
Q

What is the overall goal/function of tumor suppressor genes? What are some mechanisms to achieve this goal?

A

function: repress cell cycle/promote apoptosis

mechanisms:

1) inhibit cell division
2) initiate apoptosis following DNA damage
3) DNA repair proteins

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9
Q

What is p53?

A

tumor suppressor protein that regulates the cell cycle

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10
Q

p53 is mutated in __ % of all tumors

A

50%

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11
Q

What is the difference between proto-oncogenes and oncogenes?

A

proto-oncogenes = normal genes involved in cell growth and proliferation or inhibition of apoptosis (i.e. opposite of tumor suppressor genes)

oncogenes = cancer genes due to mutations that can increase expression

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12
Q

what are the 2 types of mutations that can cause oncogenes to form? define them.

A

1) point mutations = small-scale deletions or insertions which affect its expression
2) chromosomal translocation = 2 separate chromosomal regions become abnormally fused

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13
Q

What is the Philadelphia chromosome? what kind of cancer cells is this chromosome found in? This chromosome leads to unregulated expression of which protein?

A
  • an oncogene
  • abnormal chromosome 22 (translocation of chromo 9 and 22)
  • found in LEUKEMIA cancer cells
  • fusion –> new gene –> BCR-ABL (BCR gene from 22 and ABL from 9)
  • unregulated expression of TYROSINE KINASE ACTIVITY
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14
Q

TRUE or FALSE: Usually, MULTIPLE oncogenes and tumor suppressor genes will act in concert to cause cancer.

A

TRUE

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15
Q

1/3 of cancers can be cures with local treatment (surgery and radiotherapy); however, anti-cancer drugs are required in other cases. Why are anti-cancer drugs used instead of local treatment?

A

anti-cancer drugs address metastasis

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16
Q

When diagnosed at an advanced stage, anti-cancer drugs alone cure less than ___% of cancer patients.

A

10%

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17
Q

TRUE or FALSE: Normal tissues that proliferate rapidly (bone marrow, hair follicles, intestinal epithelium) are susceptible to damage from cytotoxic anti-cancer drugs.

A

TRUE

e.g. hair loss from chemotherapy

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18
Q

Which 2 phases of the cell cycle do MOST anti-cancer drugs interfere with?

A

S phase and M phase

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19
Q

What are 4 types of DNA Synthesis Inhibitors used to treat cancer?

A

1) pyrimidine analogues
2) purine analogues
3) alkylating agents
4) anti-folates

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20
Q

What are pyrimidine analogues? What are the nucleoside bases used? What is the mechanism? Provide an example drug and its mechanism.

A
  • DNA synthesis inhibitor
  • DNA bases = T and C; RNA bases = U and C
  • mechanism: compete with normal pyrimidine precursors for the enzyme THYMIDYLATE SYNTHASE (changes dUMP to dTMP)
  • drug: 5-FLUOROURACIL (5-FU)
  • 5-FU mechanism: must be activated to FdUMP to act as a pyrimidine analogue
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21
Q

What are purine analogues? What are the nucleoside bases used? What is the mechanism? Provide an example drug and its mechanism.

A
  • DNA synthesis inhibitor
  • DNA and RNA bases = A and G
  • mechanism: rate-limiting facto for purine synthesis (alter synthesis and function of RNA and DNA)
  • drug: 6-MERCAPTOPURINE
  • drug mechanism: inhibit enzyme PHOSPHORIBOSYL PYROPHOSPHATE AMIDOTRANSFERASE (PRPP amidotransferase) –> inhibit purine nucleotide biosynthesis and metabolism
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22
Q

What is an alkylating agent? What is the mechanism? Provide an example drug and its mechanism.

A
  • DNA synthesis inhibitor
  • mechanism:
    highly reactive compounds –> covalently link to chemical groups found in nucleic acids –> these modified nucleic acids cross-link between DNA strands –> lead to strand breakage
  • drug: CISPLATIN
  • drug mechanism: platinum analogue –> lead to cross links –> strand breakage
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23
Q

What atom of guanine is most susceptible to formation of covalent bond with alkylating agents?

A

N7

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24
Q

Which 2 phases of the cell cycle are most susceptible to alkylating agents?

(hint: alkylating agents are DNA synthesis inhibitors)

A

G1 and S

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25
Q

What is an anti-folate? What is folic acid and how is it relevant for DNA synthesis? What is its mechanism? Provide an example drug and its mechanism.

(hint: the drug name rhymes with anti-folate)

A
  • DNA synthesis inhibitor
  • folic acid = essential dietary factor converted/reduced to FH4 cofactors, which provide methyl groups for synthesis of or T or U bases (for DNA or RNA)
  • mechanism:
    • anti-folate = folic acid analogue
    • interfere with FH4 metabolism, which inhibits DNA synthesis
  • drug: METHOTREXATE
  • drug mechanism: bind with high affinity to DIHYDROFOLATE REDUCTASE
26
Q

Which phase of the cell cycle is methotrexate most effective?

(hint: methotrexate is an anti-folate)

A

S phase ( when cells are rapidly proliferating during DNA synthesis)

27
Q

What are 4 natural products that can be used to treat cancer?

A

1) vinca alkaloids
2) taxanes
3) camptothecins
4) antibiotics

28
Q

What are vinca alkaloids?

a) DNA synthesis inhibitors
b) natural product
c) tyrosine kinase inhibitors
d) hormonal anticancer agents

A

b) natural product

29
Q

What plant are vinca alkaloids derived from?

A

periwinkle plant (vinca rosea)

30
Q

What is the mechanism/function of vinca alkaloids?

A

inhibit tubulin polymerization –> disrupts assembly of microtubules involved in mitotic spindle apparatus

31
Q

What phase of the cell cycle do vinca alkaloids interfere with?

(hint: consider the function/mechanism of vinca alkaloids)

A

M phase

32
Q

What are taxanes?

a) DNA synthesis inhibitors
b) natural product
c) anti-biotics
d) anti-folates

A

b) natural product

33
Q

What plant are taxanes derived from?

A

Pacific yew tree (Taxus brevifolia)

34
Q

What is the function/mechanism of taxanes?

A

promote microtubule assembly through high affinity binding –> inhibit mitosis and cell division

35
Q

What phase of the cell cycle do taxanes interfere with?

hint: consider its function/mechanism

A

M phase

36
Q

What is an example of a taxane drug?

hint: “tax” is in its name

A

PACLITAXEL

37
Q

What are camptothecins?

a) DNA synthesis inhibitors
b) anti-folates
c) tyrosine kinase inhibitors
d) natural product

A

d) natural product

38
Q

What plant are camptothecins derived from?

A

Camptotheca acuminata tree

39
Q

What is the mechanism/function of camptothecins? (hint: name the enzyme involved)

A

DNA topoisomerase = nuclear enzyme that reduce torsional stress in supercoiled DNA (through strand breakage and re-ligation)

camptothecin function:
bind and stabilize the DNA topoisomerase –> re-ligation step inhibited –> accumulation of single-stranded breaks in DNA (cytotoxicity)

(i.e. camptothecin stops DNA topoisomerase from re-ligating the broken DNA)

40
Q

What phase of the cell cycle do camptothecins interfere with? (hint: consider its function)

A

S phase (ongoing DNA synthesis is necessary for cytotoxicity/accumulation of DNA strands)

41
Q

What are antibiotics?

a) natural product
b) DNA synthesis inhibitors
c) camptothecins
d) taxanes

A

a) natural product

42
Q

What are antibiotics derived from?

A

soil microbe Streptomyces

43
Q

What is the mechanism of antibiotics in treating cancer?

A

bind DNA through intercalation –> block DNA synthesis and cell replication

44
Q

What is an example of an antibiotic drug used to treat cancer? what are the 4 mechanisms of action?

A

drug: ANTHRACYCLINES (DOXORUBICIN)

mechanisms:

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

45
Q

What is the most widely used anticancer drug? Classify this drug fully.

A

drug: ANTHRACYCLINES (DOXORUBICIN)
class: antibiotic, natural product

46
Q

What are 3 miscellaneous anti-cancer drugs? (i.e. not natural product or DNA synthesis inhibitor)

A

1) tyrosine kinase inhibitors
2) epidermal growth factor receptor (EGFR) inhibitors
3) hormonal anticancer agents

47
Q

What is IMATINIB?

a) tyrosine kinase inhibitor
b) hormonal anticancer agent
c) epidermal growth factor receptor (EGFR) inhibitor
d) antibiotic
e) DNA synthesis inhibitor

A

a) tyrosine kinase inhibitor

48
Q

What is the mechanism of IMATINIB? (hint: consider what type of anticancer drug it is)

A

inhibit tyrosine kinase domain of the Bcr-Abl oncoprotein (Philadelphia chromo?)

49
Q

What kind of cancer does IMATINIB treat?

A

leukemia cancer

50
Q

How do epidermal growth factor receptor (EGFR) inhibitors work? (hint: solid tumors)

A
  • solid tumors are caused by OVEREXPRESSION of EGFR
  • i.e. activation of EGFR promotes cell proliferation, angiogenesis, metastasis, etc.
  • EGFR inhibitors stop excessive proliferation of cell growth
51
Q

What is CETUXIMAB?

a) tyrosine kinase inhibitor
b) hormonal anticancer agent
c) epidermal growth factor receptor (EGFR) inhibitor
d) antibiotic
e) DNA synthesis inhibitor

A

c) epidermal growth factor receptor (EGFR) inhibitor

52
Q

What is the mechanism of CETUXIMAB?

A

monoclonal antibody directed against extracellular domain of EGFR

53
Q

What is TAMOXIFEN?

a) tyrosine kinase inhibitor
b) hormonal anticancer agent
c) epidermal growth factor receptor (EGFR) inhibitor
d) antibiotic
e) DNA synthesis inhibitor

A

b) hormonal anticancer agent

54
Q

What is the mechanism of TAMOXIFEN?

A
  • selective estrogen receptor antagonist

- blocks binding of estrogen to estrogen-sensitive cancer cells in breast tissue

55
Q

What kind of cancer does TAMOXIFEN treat? (hint: remember its mechanism)

A

breast cancer

56
Q

Primary drug resistance:

a) develops spontaneously in the absence of prior exposure to anti-cancer drugs
b) develops in response to a given anticancer agent

A

a) develops spontaneously in the absence of prior exposure to anti-cancer drugs

57
Q

Acquired drug resistance:

a) develops spontaneously in the absence of prior exposure to anti-cancer drugs
b) develops in response to a given anticancer agent

A

b) develops in response to a given anticancer agent

hint: ACQUIRED drug resistance develops after you ACQUIRE the drug

58
Q

TRUE or FALSE: Many anticancer drugs are carcinogenic in nature; therefore, there is an increased risk of second malignancies.

A

TRUE

59
Q

What are 5 symptoms of anticancer treatment?

A

1) impaired immune system
2) hair loss
3) nausea
4) diarrhea
5) vomiting

60
Q

Adverse effects of anticancer treatments occur primarily in ________ _________ tissues, such as bone marrow, intestinal mucosa, and the reproductive system.

A

rapidly growing

PMCOL 200 Final (11 decks)

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