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Chemotherapy drugs > Cancer Chemotherapy 2 > Flashcards

Cancer Chemotherapy 2 Flashcards

1
Q

antimetabolites general MOA

A

compounds that mimic endogenous biochemicals required for DNA, RNA synthesis or function of key enzymes

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2
Q

what drugs are antimetabolites

A

Methotrexate (folic acid)
5-fluorouracil (pyrimidines)
6-mercaptoprurine (purines)

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3
Q

how do folic acid and methotrexate differ

A

methotrexate has an extra methyl group

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4
Q

methotrexate MOA

A

resembles folic acid and binds to DHFR

1000x affinity for DHFR than folate

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5
Q

what drugs are folic acid analogs

A

methotrexate
trimetrexate
pemetrexed

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6
Q

pemetrexed is a newer derivative of methotrexate and is better why?

A

it can directly inhibit individual enzymes in purine synthesis pathway (Thymidylate sythase, GAR and AICAR formyltransferases) as well as DHFR

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7
Q

folic acid analogs inhibit what phase of the cell cycle

A

CCS-S phase

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8
Q

what are the toxic side effects of folic acid analogs

A

hepatotoxicity
pulmonary toxicity
Oral and GI ulceration

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9
Q

how can one minimize the toxic effects of folate depletion in normal cells

A 
Leucovorin rescue (only affects non-tumor cells)
administered 24-36 hours after methotrexate
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10
Q

capecitabine is a prodrug that gets converted to what by carboxyesterases and cytidine dreaminess in the liver

A

5-FU

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11
Q

capecitabine and gemcitabine are analogs of what

A

pyrimidine

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12
Q

5-FU effects the cell cycle when

A

CCNS; C1 and S-phases

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13
Q

5-FU MOA

A

decreased DNA synthesis by inhibiting thymidylate sythase
incorporation into DNA (unstable)
incorporation into RNA (altered function)

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14
Q

what toxicities are associated with 5-FU

A

oral and GI ulceration

stomatitis and diarrhea (stop medication)

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15
Q

cytarabine effects the cell cycle when

A

CCS-S phase

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16
Q

Gemcitabine effects the cell cycle when

A

CCNS

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17
Q

MOA of cytarabine

A

inhibits DNAPol-alpha

incorporation into DNA

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18
Q

what drug inhibits DNAPol-alpha

A

cytarabine

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19
Q

what is the active form of 5-FU

A

5-FdUMP

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20
Q

what two drugs inhibit thymidylate sythase

A

5-FU

pemetrexed (PEM)

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21
Q

the metabolism of 6-mercaptopurine is inhibited by what

A

allopurinol

gotta lower dose in ppl w/ gout on this drug

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22
Q

MOA of 6-mercaptopurine

A

inhibits synthesis of adenine and guanine by blocking the conversion of inosinate to purine precursors

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23
Q

what drug is a potent “pseudo-feedback inhibitor or purine biosynthesis”

A

6-mercaptopurine

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24
Q

6-mercaptopurine effects the cell cycle where

A

CCS-S phase

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25
Q

What toxicities are associated with 6-mercaptopurine

A

cholestasis oral and intestinal ulcers

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26
Q

ADA inhibitors MOA

A

inhibit ADA directly or via metabolites- build up of adenosine and dAdenosine nucleotides decreases DNA synthesis by inhibiting ribonucleotide reductase

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27
Q

ribonucleotide reductase is inhibited by what drug

A

ADA inhibitors

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28
Q

ADA inhibitors are used to treat what

A

hairy cell leukemia

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29
Q

what drugs are tubulin-binding agents

A

vinca alkaloids

yew alkaloids

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30
Q

what drugs are vinca alkaloids

A

vincristine
vinblastine
vinorelbine

31
Q

what drugs are yew alkaloids

A

Paclitaxel (taxol)

docetaxel

32
Q

MOA of vinca alkaloids (vincristine, vinblastine, vinorelbine)

A

bind specifically to soluble tubulin to block polymerization

arrests cellular mitosis in metaphase

33
Q

vinca alkaloids (vincristine, vinblastine, vinorelbine) effect the cell cycle when

A

CCS-M phase

34
Q

what toxicity is associated with vinca alkaloids (vincristine, vinblastine, vinorelbine)

A

peripheral neuropathy
alopecia (hair loss)
SAIDH

35
Q

what drugs have SIADH as toxic side effects

A 
cyclophosphamide
vinca alkaloids (vincristine, vinblastine, vinorelbine)
36
Q

MOA of paclitaxel (and docetaxel)

A

prevents microtubule depolymerization by bind to and stabilizing polymerized tubulin

37
Q

paclitaxel (and docetaxel) effects the cell cycle when

A

CCS-M

38
Q

what toxic side effects re associated with paclitaxel (and docetaxel)

A

peripheral neuropathy (dose limiting)

39
Q

which interferon is an anti-cancer drug

A

IFN-alpha

40
Q

MOA of IFN-alpha

A

inhibits tumors by regulating the host immune system of the patient
direct activity against cancer cells

41
Q

IFN-alpha effects the cell cycle when

A

CCNS slows G1 to S and S to G2

42
Q

what cancers are hormone responsive

A

breast, endometrial, prostate

43
Q

MOA of prednisone

A

anti-inflammatory property and alter immune responses

cause apoptosis in certain leukemia cells

44
Q

prednisone is used to treat what

A

Hodgkin’s disease (MOPP), acute leukemias, relapsed hairy cell leukemia lymphomas
manage hemolytic anemia and hemorrhagic complications of lymphomas and CLL

45
Q

what drug is used to manage hemolytic anemia and hemorrhagic complications of lymphomas and CLL

A

prednisone

46
Q

Progestins (synthetic progesterones and its derivatives) MOA

A

used in hormone responsive cancers expressing progesterone receptors

47
Q

What drugs are anti estrogens

A

tamoxifen and toremefine

48
Q

anti estrogens (tamoxifen and toremefine) are used to tread what

A

estrogen receptor positive breast cancer

49
Q

what is the stipulation with anti estrogens (tamoxifen and toremefine)

A

tamoxifen is not steroid

both have week estrogen affinity

50
Q

MOA of anti-androgens (cased, eulixin, nilandron)

A

blocks androgen-induced growth

normally combined with leuprolide or other luteinizing hormone releasing hormone (LHRH) agonist

51
Q

the combination of anti-androgens with leuprolide facilitates what

A

total androgen ablation

52
Q

leuprolide (LHRH agonist) MOA

A

blocks release of luteinizing hormone from pituitary gland

53
Q

what does the suffix “mab” stand for

A

monoclonal antibody

54
Q

what is an example of ligand-independent receptor commonly found in breast cancers

A

ERBB2/Her2/Neu

55
Q

how are antibodies used in treatment of cancer

A

block cell surface receptors which promote tumor growth

block receptors which facilitate tumor angiogenesis

56
Q

ERBB1 and ERBB2 promote tumor growth how

A

constitutively active

57
Q

MOA of Bevuczimab

A

blocks VEGF and prevents angiogenesis

58
Q

MOA of Denusomab

A

blocks RANK-RANKL in bone

59
Q

MOA of Traztuzumab

A

blocker Her2/Neu

60
Q

targeted inhibitors of cancer growth work how

A

target intracellular growth pathways overexpressed/amplified in cancer

61
Q

Imatinib MOA

A

blocks Bcr-Abl kinase

62
Q

what drug has a response rate of about 100% in the chronic phase of CML

A

Imatinib

63
Q

Erlotinib,Geftinib MOA

A

blocks EGFR signaling

64
Q

Crizotinib MOA

A

blocks ALK-1 kinase

65
Q

suffix “inib” stands for what

A

inhibitor

66
Q

drugs that inhibit anti-apoptotic proteins target what

A

Bcl-2

67
Q

Venetoclax MOA

A

binds Bcl-2 and inhibits its anti-apoptotic activity

68
Q

venetoclax is approved to treat what

A

refractory chronic lymphocytic leukemia

69
Q

drugs that target epigenetic signaling target what

A

histone deacyetylases (HDACs)

70
Q

Vorinostat and Romidepsin are examples of what type of anti-cancer drug

A

HDAC (histone deacyetylase) inhibitors

71
Q

what is the normal function of PARP-1

A

rescue cells by base excision repair

72
Q

inhibition of PARP-1 leads to what

A

cellular apoptosis

73
Q

Olaparib MOA

A

PARP-1 inhibitor which leads to increased DNA damage, this damage cannot be fixed by homologous recombination with BRCA mutations are present

74
Q

Olaparib is approved for use in what

A

ovarian cancer that contains BRCA1/BRCA2

Chemotherapy drugs (2 decks)

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