Pcol Sem 2 Test 3 Chemo Packet 2

Front 1

how does 6-MP work

Back 1

converted via HGPRT into 6-TIMP which then inhibits purine synthesis

also incorporated into DNA/RNA

Front 2

how does 6-TG (thioguanosine) work

Back 2

converted via HGPRT into 6-TIMP which inhibits purine synthesis

also incorporated into DNA/RNA

Front 3

how does Fludarabine and Cladribine work

Back 3

they inhibit adenosine deaminase causing an accumulation of adenosine which results in feed back inhibition on purine synthesis

they are also incorporated into DNA and cause chain termination

also inhibit repair enzymes therefore errors in genome and repressor genes should stop cell cycle therefore apoptosis

Front 4

how does Pentostatin work

Back 4

inhibits adenosine deaminase causing an accumulation of adenosine resulting in feed back inhibition on purine synthesis

incorporated into both DNA and RNA causing strand breakage

also causes dAMP to accumulate resulting in inhibition of ribonucleotide reductase therefore no more deoxyribose and inhibits hydrolase causing accumulation of homocysteine which is toxic to lymphocytes

Front 5

how does Vinca Alkaloids work

Back 5

bind to beta tubulin block its ability to associate w/ alpha tubulin

therefore cell can't form mitotic spindle

Front 6

where does vinca alkaloid work

Back 6

M phase

Front 7

what is the resistance to vinca alkaloids

Back 7

gene amplification of MDR (exporters)
insufficient intracellular drug concentration

Front 8

what are the Taxanes

Back 8

paclitaxel
docetaxel

Front 9

what are the properties of Paclitaxel

Back 9

reaction to delivery vehicle (cremophore) therefore must give antihistamines prior to administration

Front 10

what are the properties of docetaxel

Back 10

more potent than paclitaxel
co-administered w/ glucocorticoids to avoid edema

Front 11

what are the SE of taxanes

Back 11

paclitaxel - bone marrow suppression

docetaxel - bone marrow suppression, fluid retention

Front 12

what is the MOA of Camptothecin

Back 12

Topo 1 normally makes a single stranded cut to reduce strain and the ligates the cut, but irinotecan/topotecan stabalize the the DNA enzyme complex such that the cut cannot be re-ligated

Front 13

what are the camptothecin analogs

Back 13

irinotecan
topotecan

Front 14

what phase does irinotecan and topotecan predominantly work in

Back 14

S phase

Front 15

what is the resistance mechanisms for irinotecan and topotecan

Back 15

MDR amplification, increase repair mechanism

Front 16

what are the adverse effects of camptothecins and how do you treat it

Back 16

severe diarrhea treat w/ loperamide

Front 17

what is the MOA of Actinomycin D

Back 17

intercalates into DNA and stabalizes the DNA so it can't unwind
produces free radicals

BOTH NORMAL AND CANCER CELLS ARE AFFECTED

Front 18

what are the Anthracycline antibiotics

Back 18

-rubicin

Front 19

what is the MOA of anthracycline

Back 19

intercalate into double helix (interfer w/ DNA/RNA synth)
inhibit topo 2 (inhib religation of DS breaks made to relieve coil strain)
free radical generation (damage DNA)

Front 20

what is the resistance to anthracyclines

Back 20

MDR
increased antioxidant generation

Front 21

what are the SE of anthracyclines

Back 21

myelosuppression

Front 22

what drug causes severe cardiotoxicity and why

Back 22

anthracycline due to production of free radicals from interacting w/ Iron

treat with alpha tocopherol, dexrazoxane (chelating agents)

Front 23

what is the MOA of mitoxantrone

Back 23

inhib topo 2
less free radical generation
intercalates into double helix

Front 24

what are the epipodophyllotoxins

Back 24

podophyllotoxin
etoposide
teniposide

Front 25

what is the MOA of podophyllotoxin

Back 25

binds tubulin interefers w/ mitosis

Front 26

what is the MOA of etoposide

Back 26

complexes w/ topo 2 interferes w/ strand religation

greatest activity at S and G2

Front 27

what is the MOA of teniposide

Back 27

complelxes w/ topo 2 interferes w/ strand religation

greatest activity at S and G2

Front 28

what is the resistance to epipodophyllotoxins

Back 28

amplification of MDR
mutation in topo 2 that decreases drug affinity to bind

Front 29

what is the MOA of bleomycin

Back 29

copper chelating that causes production of free radicals and causes damage to DNA

Front 30

what is the resistance to bleomycin

Back 30

upregulation of hydrolase
excess antioxidants
enhanced strand repair mechanism

Front 31

what are the SE of anthracyclines

Back 31

myelosuppression

Front 32

what drug causes severe cardiotoxicity and why

Back 32

anthracycline due to production of free radicals from interacting w/ Iron

treat with alpha tocopherol, dexrazoxane (chelating agents)

Front 33

what is the MOA of mitoxantrone

Back 33

inhib topo 2
less free radical generation
intercalates into double helix

Front 34

what are the epipodophyllotoxins

Back 34

podophyllotoxin
etoposide
teniposide

Front 35

what is the MOA of podophyllotoxin

Back 35

binds tubulin interefers w/ mitosis

Front 36

what is the MOA of etoposide

Back 36

complexes w/ topo 2 interferes w/ strand religation

greatest activity at S and G2

Front 37

what is the MOA of teniposide

Back 37

complelxes w/ topo 2 interferes w/ strand religation

greatest activity at S and G2

Front 38

what is the resistance to epipodophyllotoxins (tenopiside, etoposide, podophyllotoxin)

Back 38

amplification of MDR
mutation in topo 2 that decreases drug affinity to bind

Front 39

what is the MOA of bleomycin

Back 39

copper chelating that causes production of free radicals and causes damage to DNA

Front 40

what is the resistance to bleomycin

Back 40

upregulation of hydrolase
excess antioxidants
enhanced strand repair mechanism

Front 41

how is bleomycin given

Back 41

parenteral administration
direct installation into bladder for bladder cancer

Front 42

what are toxicity of bleomycin

Back 42

irreverisble lung fibrosis
skin problems

Front 43

what is the MOA of L-asparaginase

Back 43

degrades circulating asparagine

Front 44

what is the role of EGF

Back 44

upregulated,amplified, or mutated in cancer and makes the cancer more aggressive

Front 45

what are the tyrosine kinase inhibitors

Back 45

gefitinib
imatinib

Front 46

what are the EGF antibodies

Back 46

trastuzumab
cetuximab
pertuzumab

Front 47

what are the MT stabilizers

Back 47

taxanes (paclitaxel, docetaxel, carbazitaxel) ixabepilone

Front 48

what are the MT destabilizers

Back 48

vinca alkaloids (vinblastine, vinorelbine, vincristine)