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Year 2 Pharmacology > Antineoplastic agents I > Flashcards

Antineoplastic agents I Flashcards

1
Q

are tumor cells with shorter doubling time easier or more difficult to treat?

A

easier

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2
Q

cell kill hypothesis

A

chemotherapy drugs kill a constant proportion of cells, not a constant number - first order kinetics

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3
Q

defintion: epithelial-mesenchymal transition

A

a process by which cell lose adhesive properties and become motile (leads to metastasis and drug resistance)

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4
Q

how do the cytotoxic cancer drugs work?

A
  1. perturbing normal DNA replication
  2. perturbing mitosis
  3. starving cells of amino acids
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5
Q

how do the targeted cancer drugs work?

A
  1. perturbing hormone and growth factor signaling
  2. inhibiting blood supply to tumor
  3. targeting activating proteins responsible for tumor growth
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6
Q

what is the classification of adenine and guanine?

A

purine bases

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7
Q

what is the classification of thymine, cytosine, and uracil?

A

pyrimidine bases

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8
Q

what is the classification of adenosine and guanosine?

A

purine nucleosides

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9
Q

what is the classification of thymidine, cytidine, and uridine?

A

pyrimidine nucleosides

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10
Q

what is the classification of AMP and GMP?

A

purine nucleotides

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11
Q

what is the classification of TMP, CMP, and UMP?

A

pyrimidine nucleotides

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12
Q

what is the goal of the antimetabolite cancer drugs?

A

inhibiting de novo nucleotide biosynthesis

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13
Q

what is required for the conversion of purine precursors to inosine monophosphate (IMP)?

A

folate

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14
Q

what is the general mechanism of action for methotrexate?

A

inhibits dihydrofolate reducatse - reduces precursors for RNA and DNA synthesis

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15
Q

what are the main therapeutic uses for methotrexate?

A
  1. ALL in children

2. osteosarcomas (high doses)

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16
Q

following methotrexate with which drug reduces toxicity?

A

leucovorin

17
Q

what are the mechanisms of resistance against methotrexate?

A
  1. impaired transport
  2. DHFR with decreased affinity to methotrexate
  3. elevated HDFR expression
18
Q

what are the toxicities of methotrexate?

A
  1. interstitial pneumonitis
  2. nephrotoxic
  3. bone marrow suppression
19
Q

what is the general mechanism of action for 5-fluorocuracil?

A
  1. incorporated into DNA and RNA - inhibits synthesis and function
  2. inhibits thymidylate synthetase - reduces precursors
20
Q

what are the adverse effects of 5-fluorouridine?

A

oral and GI ulcers

21
Q

what does capecitabine do?

A

prodrug of 5-FU that has improved oral bioavailability allowing it to be given orally

22
Q

cytarabine is used for what type of cancer?

A

AML

23
Q

what is the general mechanism of action of cytarabine?

A
  1. incorporates into DNA and RNA

2. inhibits DNA polymerase

24
Q

cytarabine is only active in which phase of the cell cycle?

A

S phase

25
Q

which enzyme is important for activation of Ara-C (cytarabine)?

A

deoxycytidine kinase

26
Q

what is the role of cytidine deaminase?

A

inactivates Ara-C (cytarabine)

27
Q

what are the toxicities of cytarabine?

A
  1. cerebellar syndrome

2. myelosuppression

28
Q

what are the features of cerebellar syndrome?

A
  1. dysarthria
  2. nystagmus
  3. ataxia
29
Q

why does cytarabine cause cerebellar syndrome?

A

gets to high levels in the CNS because dytidine deaminase levels are low in the CNS

30
Q

what is the primary resistance mechanism of cytarabine?

A

loss of deoxycytidine kinase

31
Q

upregulation of which enzyme leads to inactivation of Ara-C and resistance against cytarabine?

A

cytidine deaminase

32
Q

what is the mechanism of action of gemcitabine?

A
  1. incorporates into DNA, inhibits synthesis

2. inhibits ribonucleotide reductase - reduces precursors

33
Q

what is the the mechanism of resistance for gemcitabine?

A

reduced activity of deoxycytidine kinase

Year 2 Pharmacology (70 decks)

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