Exam 4; Cancer Chemotherapy Flashcards
What is the definition of neoplasia
uncontrolled growth of cells
What are three treatments of neoplasias
surgery
radiation
pharmacologic agents
Non-specific cancer agents act on what
all cell phases of replication and resting
Cell specific cancer agents act on what
all cell that are replicating rapidly
Cell specific cancer agents act on more defined sites like what
antimetabolites
mitotic spindle inhibitors
enzyme inhibitors
What is the broad scope of cell cycle non-specific agents
alkylating agents
What is the mechanism behind the alkylating non-specific agents
adding an alkyl group to DNA, causing DNA cross linking and inhibits cell replication and RNA synthesis
What is the mechanism behind cyclophosphamide
pro-drug given orally or IV
when it kits the cell/DNA it stops the cell from working
What type of drug is lomustine
pro-drug given IV; alkylating agent
What are some side effects of cisplatin
renal damage and ototoxicity
What type of drug is cisplatin
alkylating agent
What is the mechanism behind doxorubicin
inserts itself into DNA and blocks DNA and RNA synthesis
Doxorubicin and other rubicin’s produce these
free radicals; can break DNA strands
Doxorubicin can cause this to occur
heart muscle degeneration (due to the free radicals)
How is doxorubicin given
IV
What is the mechanism behind dactinomycin
intercalates with DNA and interferes with mRNA synthesis
What is the mechanism behind bleomycin
intercalates with DNA and causes DNA strand breakage
What can result from bleomycin
pulmonary fibrosis
What is the mechanism behind cell cycle specific agents
block the specific enzymatic pathways in DNA synthesis; inhibit cell synthesis; ENZYME INHIBITORS
What is the mechanism behind methotrexate
inhibits dihydrofolate reductase
Methotrexate can cause this to happen
myelosuppression (bone marrow)
What can be used to treat the side effect caused by methotrexate
giving leucovorin, which is a THFA analog; which can resume normal cells but not malignant
What is the mechanism behind 5-flurouracil
it inhibits thymidylate synthase; inhibit thymidine synthesis
What is the mechanism behind cytarabine
inhibits DNA polymerase
What type of drugs are 5-flurouracil and cytarabine
pyrimidine analogs
What is the mechanism behind 6-mercaptopurine
its converted to an analog that inhibits several enzymes needed for purine synthesis
What type of drugs are the pyrimidine and purine analogs
pro-drugs
What is the mechanism behind vincristine and vinblastine
binds to microtubules and blocks cell mitosis; given IV
What is the mechanism behind paclitaxel and the other “taxel’s”
forms abnormal microtubules
What is the mechanism behind Eribulin
inhibits microtubule and prevents mitosis; causing apoptosis
What is the mechanism behind ixabepilone
binds microtubules
What is the mechanism behind etoposide
inhibits topoisomerase II causing un-repairable DNA breaks
What is the mechanism behind topotecan (and irinotecan)
topoisomerase I inhibitor
What is the mechanism behind flutamide and the other “lutamides”
blocks the androgen receptor
What is the mechanism behind abiraterone
it inhibits the enzyme 17-hydroxylase lyase (CYP17)
inhibit androgen synthesis
What is the mechanism behind leuprolide
receptor activator; stimulates the GnRH receptor
What is the mechanism behind tamoxifen (and fluvestrant)
blocks the estrogen receptor
What are two side effects of tamoxifen
retinal changes
increased cataract formation
What is the mechanism behind anastrozole
inhibits the enzyme aromatase, which is responsible for converting testosterone to estrogen
What is the mechanism behind prednisone
inhibits the immune system functions, therefore used to treat neoplasia of the immune system such as leukemias and lymphocytes
Most of the new cancer drugs target this
kinase; they are KINASE INHIBITORS
How can you distinguish the kinase inhibitors from the other drugs
they end in “-nib”
What is the mechanism behind imitinib
protein kinase inhibitor, it inhibits the kinase responsible for inhibiting apoptosis (therefore letting apoptosis happen)
What is imitinib used to treat
chronic myelogenous leukemia (CML)
What is the route of imitinib administration
orally, and has relatively few side effects (edema is possible)
What kind of side effects to the -nib drugs have
relatively few, since they are so specific
What is the mechanism behind bortezomib and carfilzomib
they inhibit proteasome which allow the buildup of proteins, killing the cell
What condition is treated with bortezomib and carfilzomib
multiple myeloma; overproduction of bone marrow cells
How are monoclonal antibodies more and less specific at the same time
more specific in that they can target any molecule
less specific in that you can’t predict the impact
What is the mechanism behind trastuzumab
directed against a kinase; VesHER2 (human epidermal growth factor receptor)
What is the mechanism behind bevacizumab
blocks VEGF (vascular endothelial growth factor) preventing the growth factor from binding to its receptor
How does bevacizumab destroy the tumor
tumors only grow if there is a blood supply, VEGF (of which is blocked by bevacizumab) allows the growth of blood vessels in tumors
What is the mechanism behind rituximab
MAB vs CD20, a receptor that allows the binding and control of immune cells
What conditions does rituximab treat
chronic lymphocytic leukemia
RA
What are six problems with the use of traditional DNA binding agents to treat neoplasia
not all cancer cells divide rapidly
normal cells are affected by neoplastic agents
not all cancer cells will be killed by the drug
cancer cells can become resistant to the drug
drugs may not enter the CNS
the alkylating agent themselves may cause neoplasia
True or False
a combination of cancer drugs is less effective than one targeted drug
False, the combo may be more effecting
What are five successes of disease with cancer therapy
chroiocarcinoma ALL Hodgkin's testicular osteosarcoma
What are four cancers that have improved survival rates due to new drugs
breast
ovarian
colon
multiple myeloma