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125 Cards in this Set

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thrombocytopenia
decrease in platelets
leukocytopenia
decrease in WBCs
doubling time of Ca cells? of normal cells?
50-80 days
how many cells present when tumor is first palpable?
10 to the 10
skipper's log kill hypothesis
chemo kills by first order kinetics so can only kill a set % of cells each round
resistance via insufficient drug uptake by cell
methotrexate
daunomycin
resistance via insufficient activation of drug
6-mercaptopurine
5-Fu
resistance via increased inactivation
arabinosyl cytosine
resistance via increased concentration of target enzyme (gene amplification)
methotrexate
resistance via decreased requirement for a specific metabolic product
L-asparaginase
resistance via increased utilization of an alternative pathway (salvage)
antimetabolites
resistance via rapid repair of drug-induced lesions
alkylating agents
resistance via increased efflux of drug (p-glycoprotein pump, multi-drug resistance)
natural products
phase I trials
toxicology
phase II trials
standard doses (find responsive Ca)
phase III trials
compare to standard therapy
Gleevec
for CML
inhibits oncogene
Avastin
anti-angiogenesis
how is mustargen given?
IV b/c lots of vesicant activity
Mustargen use
Hodgkin's and other lymphomas
melphalan is cool because?
alkylating agent that can be given orally (b/c of phenyl ring)
chlorambucil is cool because?
lease toxic nitrogen mustard
melphalan use
multiple myeloma
ovarian and breast ca
chlorambucil use
chronic lymphocytic leukemia
cytoxan (cychophosphamide) is given?
orally--must be metabolized
toxicity of cylophosphamide
bladder and bone marrow
cylophosphamide use
leukemia and lymphoma
action of alkylating agents
bind directly to DNA to prevent DNA unwinding, causes DNA breaks
MESNA
binds acrolein in bladder to prevent toxicity when getting cytoxan or ifosfamide
ifosfamide
isomer of cytoxan
use of ifosfamide
osteosarcoma
drawback of ifosfamide?
more bladder toxicity
thiotepa
alkylating agent
used for recurrent bladder cancer
busulfan (myleran)use
CML
toxicity of busulfan
not much
nitrosureas given
orally, require in vivo activation
streptozocin
nitrosurea
used for pancreatic islet cell carcinoma
triazene use
melanoma
methotrexate is an analog of
folic acid
tetrahydrofolate necessary for
1 carbon transfer reaction (synthesis of DNA)
toxicity of methotrexate
infection
GI hemorrhage
glossitis
stomatitis
uses of methotrexate
choriocarcinoma
leukemia and lymphoma
sarcoma
psoriasis
breast head and neck
arthritis
if using high dose methotrexate, need what
leucovorin resuce
leucovorin action
provides tetrahydrofolate to rescue cells when undergoing methotrexate therapy
5-Fu's mechanism of action (via intermediates)
1. forms 5-dUMP - inhibits thymidilate synthase
2. forms 5-FUTP - can be incorporated into RNA
5-Fu is an analog of
uracil
why cancer cells susceptible to 5-Fu
cancer cells convert 5-Fu to 5-Fdump faster than normal cells do
role of leavocorin with 5-Fu
stabilizes thymidylate synthetase and 5-FduMP complex
uses of 5-Fu
breast, GI, head and neck
+leavovorin for colon
how 5-Fu given
iv
cytabarine/Ara-C analog of
2' deoxycytidine
action of cytabarine
inhibits DNA polyermase and ribonucleoside diphosphate reducatase
does cytabarine require metabolism
yes-- by deoxycytidine kinase
resistance to cytabarine
usually from increased activation by cytidine deaminase
use of cytabarine
acute leukemia
6-mercaptopurine analog of
hypoxanthine
does 6-mercaptopurine need to be activated
yes
6-mercaptopurine's mechanism of action
inhibits purine nucleotide synthesis and metabolism
use of 6-mercaptopurine
acute leukemia
how is 6-mercaptopurine given
oral
imuran's use
immunosuppressive to prevent rejection
imuran's structure
like 6-mercaptopurine
allopurinol is
analog of hypoxanthine
action of allopurinol
inhibits xanthine oxidase (and so conversion of purines to uric acid)
toxicity of allopurinol
makes toxicities of purine analogs (6-mercaptopurine and imuran) worse
action of Vincristine (oncovin) and vinblastine (velban)
bind to tubulin to cause metaphase arrest (M phase specific)
toxicity of vinblastine
myelosuppression
toxicity of vincristine
peripheral neuropathy
use of vincristine
Hodgkin's, acute leukemia
use of vinblastine
testicular ca, neuroblastoma, lymphoma
etoposide's action
inhibits topoisomerase II (S and G2 phase)
taxol's action
prevents depolymerization of microtubules (M phase specific)
use of Taxol
ovarian and breast cancer
toxicity of Taxol
peripheral neuropathy
myelosuppression
excretion of natural products v. alkylating agents/antimetabolites
natural products = liver (bile)
alkylating agents/antimetabolites = kidneys
mechanism of action of Actinomycin D
intercalates b/w adjacent base pairs of DNA
inhibits DNA dependent RNA polymerase
cycle specificity of actinomycin D
none
use of actinomycin D
Wilm's Tumor
rhabdomyosarcome
choriocarcinoma
testicular cancer
daunorubicin and adriamycin mechanism of action
intercalation of DNA
produces O2 radiacals, which damage DNA
toxicity of adriamycin
heart
red urine
use of adriamycin
solid tumors and leukemia
mitoxantrone
like anthracylines but less cardiac toxicity
bleomycin's mechanism of action
causes oxidative release of bases and DNA strand breaks
toxicity of bleomycin
lung (pulmonary fibrosis)
hyperpigmentation of skin
bone marrow sparing
use of bleomycin
testicular cancer
squamous cell carcinomas
lymphoma
mitomycin C mechanism
metabolically activated to become alkylating agent
use of mitomycin C
gastric cancer
prednisone's mechanism of action
lympholytic
use of prednisone
lymphocytic leukemia and lymphoma
mechanism of leuprolide
blocks release of ganadotropin (LH)
use of leuprolide
prostate cancer
use of flutamide
prostate cancer
mechanism of flutamide
blocks androgen receptor
toxicity of leuprolide
hot flashes
loss of lipido
causes initial disease flare sometimes
toxicity of flutamide
diarrhea
liver toxicity
mechanism of proscar
blocks 5 alpha reductase (and so conversion of testosterone to DHEA)
side effect of aromatase inhibitors
loss of bone density
examestane use
breast cancer
mechanism of examestane
blocks aromatase
mechanims of progestins
down-regulates estrogen
toxicity of progestins
menstrual bleeding
edema
use of progestin
endometrial cancer
use of somatostatin
pancreatic islet cell tumor
use of asparaginase
lymphocytic leukemia
toxicity of asparaginase
hypersensitivity
liver and CNS
*bone marrow spared*
cisplatin mechanism
alkylating
phase specificity of cisplatin
none
use of cisplatin
testicles, head, neck, ovary, cervix, bladder, lung
toxicity of cisplatin
kidney
ototoxicity
peripheral neuropathy
advantage of carboplatin
like cisplatin but less renal toxicity
mechanism of procarbazine
denatures DNA
use of procarbazine
Hodgkin's, lymphomas, lung, brain
how is procarbazine given
oral
mechanism of hydroxyurea
blocks ribonucleotide disphosphate reductase (and so DNA synthesis)
phase specificity of hydroxyurea
S
hydroxyurea antagonizes what
5-FU
use of hydroxyurea
leukemia
MOPP is
mustargen (mecholerhamine)
oncovin (incristine)
procarbazine
prednisone
MOPP used for
Hodgkin's
BVP use?
testicular cancer
BVP composition
bleomycin
vinblastine
platinum
CMF use
breast cancer
CMF composition
cyclophosphamide
methotrexate
5-FU
FAM use
gastric cancer
FAM composition
fluorouracil
adriamycin
mitomycin C