Oncology deck Flashcards
cetuximab & panitumumab
- MoA
- uses
- contraindications
- monoclonal antibodies that function as EGFR inhibitors
- used in stage 4 colorectal cancer (WT KRAS) + head/neck cancer
**have to test patient for presence of KRAS gain-of-function mutation before you begin them on this therapy (presence of KRAS-activating mutation will make this therapy ineffective since KRAS is downstream of EGFR)
rituximab
- MoA
- uses
- contraindications
- monoclonal antibody that inhibits CD20 on B cell surface
- used for B cell lymphomas (non-hodgkin’s), CLL, ITP, and RA
**can cause reactivation of JC virus –> progressive multifocal leukoencephalopathy in patients
denosumab
- MoA
- uses
**basically functions the same way as endogenous osteoprotegrin!!
- binds to RANKL receptor on osteoblasts to prevent it from binding to RANK on osteoclasts –> no osteoclast activation
- used to decrease bone metastases in cancers that frequently invade skeleton (PBKTL=prostate, breast, kidney, thyroid, lung)
tamoxifen & raloxifen
- MoA
- uses (including patient population)
- adverse effects
-both classified as SERM’s (selective estrogen receptor modulators) due to differential effects, depending on the tissue
- both are antagonists in the breast + agonists in the bone; tamoxifen is also an agonist in the endometrium whereas raloxifen is an antagonist
- tamoxifen is used for ER+ and/or PR+ breast cancer, specifically in PRE-menopausal women
- raloxifen is used for osteoporosis (elderly females)
- tamoxifen increases risk of endometrial carcinoma
- both increase risk of thromboembolic events (estrogen is a pro-coagulant)
anastrozole & lansoprazole
- MoA
- uses (including patient population)
-peripheral aromatase inhibitors –> inhibit estrone formation
- used for ER+ and/or PR+ breast cancer in POST-menopausal patients (main source of estrogen is from peripheral aromatase)
- *use this instead of tamoxifen because of the similar efficacy in decreasing estrogen levels but has no risk of endometrial carcinoma like tamoxifen does
- CANNOT be used for pre-menopausal women because it is a COMPETITIVE antagonist of aromatase and the ovaries make such a large amount of aromatase enzyme that it will be able to easily outcompete the drug and continue synthesizing large amounts of estrogen from ovaries
trastuzumab (herceptin)
- MoA
- uses
- adverse effects
- monoclonal antibody that binds to HER2 tyrosine kinase receptors to inhibit growth of HER2+ breast cancer cells
- also helps induce antibody-mediated cytotoxicity of the cancer cells themselves
- main use=HER2+ breast cancer
- can also be used for gastric cancer
-main adverse effect=cardiotoxicity!
(heart-ceptin!)
vemurafenib
- MoA
- uses
-specifically used for V600E mutation in the BRAF proto-oncogene, which is present in a percentage of patients with metastatic melanoma
rasburicase
- MoA
- uses
- functions as a uricase/uric acid oxidase enzyme (not normally present in humans but present in bacteria) to oxidize uric acid to its more soluble form, allantoin, for excretion
- used for prevention & treatment of tumor lysis syndrome
imatinib
- MoA
- uses
- BCR:ABL fusion protein kinase inhibitor
- used for CML, which is associated with 9:22 chromosomal translocation –> BCR:ABL fusion protein production
ruxolitinib
- MoA
- uses
-JAK1/2 non-receptor tyrosine kinase inhibitor
- used for all forms of chronic myelogenous proliferative disorders since these are all caused by over-activation of JAK2 –> excessive STAT activation and translocation to nucleus
- *works on all EXCEPT for CML (no JAK1/2 mutation here)
cladribine (2-CDA)
- MoA
- uses
- side effects
- adenosine deaminase inhibitor –> causes buildup of adenosine, which is directly lymphotoxic + throws off nucleotide pool balance in B cells –> apoptosis
- also inhibits DNA polymerase and causes DNA strand breaks
- used in hairy cell leukemia (mature CD20+ B cell neoplasm)
- nephotoxicity and neurotoxicity
**essentially a medication that causes the same defect that SCID patients inherit, which is why they have no B or T cells
doxorubicin
- MoA (3)
- uses
- toxicity & prevention
MoA:
- inhibits topoisomerase II –> inability to replicate DNA and apoptosis
- generates free radicals that damage cancer cell DNA
- also can intercalate into DNA strands directly
Uses:
- solid tumors
- leukemias
- lymphomas
Toxicity:
- cardiotoxicity is the main side effect; leads to dilated cardiomyopathy
- *give dexrazoxane (iron chelating agent) to prevent this
vincristine and vinblastine
- MoA
- adverse effects
MoA:
-bind to beta tubulin subunits and prevent them from polymerizing into microtubules –> prevent separation of chromosomes in mitosis –> inability to replicate and cell death
Adverse effects:
- vincristine causes peripheral neuropathy (inhibition of the microtubules in neurons, preventing movement of intracellular organelles and neurotransmitter delivery)
- vinblastine BLASTS the bone marrow (myelosuppression)
paclitaxel (and other taxols besides vincristine & vinblastine)
- MoA
- uses
- adverse effects
MoA:
-binds to polymerized microtubules to inhibit their DISASSEMBLY –> arrests chromosomes in M phase of mitosis
Uses:
-ovarian and breast carcinoma
Adverse effects:
-besides the usual, it can cause hypersensitivity rxn
capecitabine
- MoA
- adverse effects
MoA:
- oral form of 5-FU (normally given IV); gets converted to 5-FU in the body
- same function
Adverse effects:
-Hand foot mouth syndrome (painful sores that arise and may be dose-limiting in some patients, depending on the level of severity)
