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pcol350 final > Lui Lectures > Flashcards

Lui Lectures Flashcards

1
Q

cell cycle specific drugs

A

antimetabolites (S), vinca alkaloids(M), antibiotics, taxanes (M)
-for replicating (ex/ hematologic)

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2
Q

cell cycle non specific drugs

A

alkylating agents, antibodies, anthracyclines, antitumor antibioitcs, platinum analogs (“platin”)
replicating and non

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3
Q

log kill

A

constant fraction of cells, first order

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4
Q

may need irradiation of craniospinal axis or intrathecal drugs for

A

tumors finding sanctuaries in tissues, such as CNS

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5
Q

drugs combined at full doses

A

different toxicities, different sites of action and mechanisms

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6
Q

resistance minimized by

A

short term, intensive, intermittent therapy with drug combos

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7
Q

responsible for miltidrug resistance

A

p glycoprotein due to atp dependent pumping of drugs out of cell

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8
Q

neoplasms arising from chemo common in

A

alkylating agents

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9
Q

antimetabolite action

A

inh DNA synthesis

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10
Q

antibiotics action

A

damage or alter DNA and RNA structure

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11
Q

topoisomerase inh action

A

inhibit topoisomerase mediated religation of DNA breaks

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12
Q

alkylating agents action

A

damage or disrupt DNA and RNA structures

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13
Q

microtuble inhibitorsaction

A

disrupt mitosis

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14
Q

steroid hormones and antagonists action

A

interfere with transcription

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15
Q

monoclonal antibodies action

A

block function of targeted protein, alter function of cnacer cells and or induce cytotoxicity

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16
Q

biological response modifiers action

A

interfere with signal transduction pathways (IFN, IL)

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17
Q

tyrsine kinase inhibitors action

A

interfere with signal transduction pathways

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18
Q

proteosome inhibitors action

A

inhibit proteosome

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19
Q

angiogenesis inh action

A

disrupt tumor vasculature

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20
Q

differentiating agents action

A

allow leukemic promyelocytes to become neutropuls (all trans retinoic acid)

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21
Q

antimetabolite action

A

inh DNA synthesis; interfere with normal purine and purimidine nucleotide precursors and inhibit their synthesis and compete. S phase

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22
Q

differentiating agents action

A

allow leukemic promyelocytes to become neutropuls (all trans retinoic acid)

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23
Q

methotrexate

A

antimetabolite, related to folic acid (antagonist), inhbits dihydrofolate reductase and decreases biosynthesis of AGT and methionine and Serine
-low dose is anti inflam and immuno suppressive

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24
Q

only antimetabolite that doesn’t need conversion to become active

A

methotrexate

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25
pemetrexed
methotrexate analog
26
antibiotics
doxorubicin, daunorubicin, dactinomycin, bleomycin
27
anthracycline antibiotics
- doxorubicin (one of most widely used) and daunorubicin - used in drug combos - intercalate into DNA and block synthesis, generate oxygen radicals - cardio tox or heart failure possible
28
mixture of copper chelating glycopeptides that scize DNA oxidatively, G2
bleomycin
29
cardiac tox or heart failure
doxorubicin and daunorubicin
30
pulmonary toxicity (fibrosis)
bleomycin
31
etoposide/teniposide
topoisomerase inh, complex with DNA, prevent re ligation
32
alkylating agents action
damage or disrupt DNA and RNA structures- covalent alkylation, lethal, cell cycle non specific
33
microtuble inhibitors action
disrupt mitosis through mitotic spindle
34
etoposide/teniposide
topoisomerase inh, complex with DNA, prevent re ligation
35
can lead to secondary malignancy- mutagenic and carcinogenic
alkylating agents
36
mechlorethamine
nitrogen gas in war, causes lymphocytopenia, alkylating agent, slow
37
cyclophosphamide
most common alkylating agent, biotransformed to active compound which alkylates DNA
38
alkylating agent used to treat brain cancer (cross BBB)
nitrosureas, temozolomide
39
alkylating agents that crosslink DNA
cisplatin and carboplatin
40
responsible for multidrug resistance
p glycoprotein due to atp dependent pumping of drugs out of cell
41
monoclonal antibodies action
block function of targeted protein, alter function of cancer cells and or induce cytotoxicity
42
alkylating agents that crosslink DNA
cisplatin and carboplatin
43
vinca alkaloids
block mitosis in metaphase, bind tubulin (GTP dependent),
44
taxanes
promote polymerization and stabilization of polymer rather than disassembly- favor formation of microtubulin, chromosome separation doesn't occur -paclitaxel, docetaxel
45
taxanes
promote polymerization and stabilization of polymer rather than disassembly- favor formation of microtubulin, chromosome separation doesn't occur -paclitaxel, docetaxel
46
tamoxifen
prevents estrogen stimulation of breast cancer cells, estrogen antagonist -toremifene similar
47
fulvestrant
destroys estrogen receptors
48
prednisone
synthetic, potent, anti inflam, corticosteroid with less mineralcorticoid. - for lymphoma and acute lymphocytic leukemia - inhibit leukocytes, antibodies, inflam and lymp stuff
49
prednisone
synthetic, potent, anti inflam, corticosteroid with less mineralcorticoid. - for lymphoma and acute lymphocytic leukemia - inhibit leukocytes, antibodies, inflam and lymp stuff
50
prednisone
synthetic, potent, anti inflam, corticosteroid with less mineralcorticoid. - for lymphoma and acute lymphocytic leukemia - inhibit leukocytes, antibodies, inflam and lymp stuff
51
biological therapy
uses human defense system, stimulate immune system for destruction of malignant cells, may risk autoimmune and other tox due to specificity -cytokines, monoclonal antibodies, vaccines
52
muro
murine antibodies
53
zu
humanized antibodies
54
xi
chimeric antibodies
55
informers; ID malignancies by CDC (complement cytotoxicity) and ADCC (antibody dependent cell mediated cytotoxicity), block selected growth factors
monoclonal antibodies
56
used as biological missiles to carry radio pharmaceutical or biological toxin to cancer cells
monoclonal antibodies
57
targets extracellular hEGF (human epidermal growth factor) receptor protein 2 (HER2)
trastuzumab
58
anti epidermal growth factor targetted anti-EGFR, used for 1st line metastatic colorectal cancer, head and neck cancer
cetuximab
59
agonist against CD20
rituximab/ofatumumab
60
anti vascular endothelial growth factor (VEGF); anti angiogenesis, 1st line metastatic colorectal cancer
bevacizumab
61
anti vascular endothelial growth factor (VEGF); anti angiogenesis, 1st line metastatic colorectal cancer
bevacizumab
62
biological response modifiers
IL2 (produced by T, growth factor, can be single agent or combo) and IFN (modulate immune responses, cell mediated cytotox, regulate differentiation and expression, *have antiviral activity -both for many malignancies
63
"tinib"
tyrosine kinase inhibitors
64
imantinib
tyrosine kinase inhibitor - signal transduction inhibitor - targets *BCR-ABL (mutations in this lead to resistance)
65
geftinib
tyrosine kinase inhibitor - EGFR inh; inhibits ATP binding - low response rate
66
oral VEGF receptor 2 tyrosine kinase inhibitors
sunitinib, sorafenib
67
proteosome inhibitor that permits cell death in neaplastic cells
bortezomib
68
VEGF
best studied pro angiogenic factor; elevated elvels=prognosis and increased risk of metastasis
69
bevacizumab, vandetanib, thalidomide, lenalidomide
disrupt tumor vasculature associated with VEGF
70
all trans retinoic acid (ATRA, tretinoin)
drives leukemic promyelocytes to be mature neutrophils for APL treatment

pcol350 final (3 decks)

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