Antineoplastic Agents I Flashcards
cyclophosphamide
nitrogen mustard
-alkylating agent
ifosfamide
nitrogen mustard
-alkylating agent
busulfan
alkyl sulfonate
-alkylating agent
cisplatin
platinum coordinate complex
-alkylating agent
methotrexate
folic acid analog
-antimetabolite
fluorouracil
5-FU
pyrimidine analog
-antimetabolite
mercaptopurine
6-MP
purine analog
-antimetabolite
vinblastine
vinca alkaloid
-natural product
vincristine
vinca alkaloid
-natural product
paclitaxel
taxane
-natural product
etoposide
epipodophyllotoxin
-natural product
doxorubicin
antibiotic
-natural product
blemoycin
anthracenedione
-natural product
L-asparaginase
enzyme
-natural product
imatinib
protein kinase inhibitor
-misc agent
trastuzumab
monoclonal Ab
-misc agent
leucovorin
rescue agent
mesna
rescue agent
ondansetron
serotonin antagonist
-used to minimize adverse effects
curable by chemo
ALL AML ewing hodgkin non-hodgkin DLBCL wilms
causes of cancer
radiation
carcinogens
Hep B and C, HIV, HPV, EBV
and genetic predisposition
primary induction treatment
first treatment given
neoadjuvant therapy
given before primary tx
-to shrink tumor
type of induction therapy
cancer for which alternative therapy exists but less effective
adjuvant therapy
given after primary treatment
-lower risk cancer will come back
primary induction chemotherapy
as primary treatment
- pt with no alternative
- may be curative - hodgkin/NHL, AML, germ cell cancer
G1 phase
synthesis of components for DNA synthesis
S phase
DNA synthesis
G2 phase
synthesis of components for cell division
M phase
cell divides to two daughter G1 cells
activity of CDK and P16,p53 involved in transition of cell cycle
cell cycle specific
cytotoxic during specific phase of cell cycle
cell cycle nonspecific
cytoxic regardless of whether cell is cycling or resting (G0)
CCS drugs
antimetabolites taxanes vinca alkaloids camtothecins epipodophyllotoxins antitumor antibiotics - blemoycin
CCNS drugs
alkylating agents anthracyclines antitumor antibiotics antimetabolites - cladribine platinum analogs
S phase CCS
antimetabolites and camptothecins
S-G2 phase CCS
epipodophyllotoxins
-etoposide
G2-M phase CCS
blemoycin
M phase CCS
taxanes
vinca alkaloids
growth fraction
ration of proliferating cells to cells in G0 phase
solid tumors
lower growth fraction than disseminated cancers
increase of growth fraction
can be induced by surgery or radiation
-make more susceptible to antineoplastic chemo agents
burkitt lymphoma
100% growth fraction
-curable with chemo
trophoblastic choriocarcinoma
100% growth fraction
-curable with chemo
lung and colon cancer
slow growing
-10% growth fraction
true cure
eradication of every cancer cell
indications for chemo
tumor not amenable to surgery
-also as supplemental treatment to prevent metastasis with surgery/radiation
log cell kill hypothesis
chemo kills fraction of drugs
-first-order kinetics
three-log cell kill - 10^12 to 10^9
pharmacologic sanctuaries
regions where tumors cells less susceptible to antineoplastic agnents
interior of solid tumors or CNS, testes
may require localized radiation or surgical resection
intermittent high dose therapy
most common
allows recovery of normal tissue
more effective with CCNS drugs
continuous infusion therapy
drugs metabolized/excreted more effective
also CCS drugs more effective this way
routes of administration for chem
IV and PO
colorectal cancer
mets to liver - use intraarterial perfusion of chemo drugs to cathgeter in hepatic artery
lt route of admin**
drug combo
benefits -
1 maximal cell killing within range of tolerated toxicity
2 effective against broader range of clones with different genetic abnormalities
3 may delay or prevent development of drug-resistant tumors
