Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
34 Cards in this Set
- Front
- Back
"o"mab
"xi"mab "zu"mab "u"mab |
o = mouse monoclonal antibody
xi = chimeric monoclonal antibody zu = humanized monoclonal antibody u = human monoclonal antibody |
|
tyrosine kinase inhibitors (TKI) MOA
"-inib" |
competatively bind to ATP-binding pocket and inhibit their kinase activity
|
|
26S proteosome inhibitor
"-omib" |
Inhibition of a chymotrypsin-like proteolytic activity of the 26S proteasome activity
|
|
bortezomib..MOA and AE. what type of cancers?
|
reversible inhibitor of 26S proteosome (specifically chymotrypsin)
multiple myelomas and lymphoma inhibits degradation of ubiquinated proteins including tumor suppressors (so increased conc. of tumor suppressors) AE: thrombocytopenia, neutropenia, anemia |
|
explain PI3K pathway of tyrosine kinase receptors
|
PI3K = SURVIVAL!!
PIP3 activates AKT by facilitating its phosphorylation by PDPK1 and PDPK2 (mtorC2). AKT, in turn, activates mTOR which creates proteins for cell growth, proliferation, and survival. PTEN regulates activity of the PI3K pathway by converting PIP3 back to PIP2. |
|
explain MAPK pathway of tyrosine kinase receptors
|
MAPK = PROLIFERATION!
RAS, RAF, MEK, and ERK are activated by sequential kinase activity. Both the pathways regulate multiple cellular processes vital for the malignant cell. Ligand binding and, therefore, downstream activation are blocked by EGFR MoAb. The most common aberrations leading to inappropriate activation of the pathways in cancer cells are also depicted. |
|
anti EGFR therapies: monoclonal antibodies
|
cetuximab, panitumumab
|
|
small molecule inhibitors (TKI)
|
lapatinib, erlotininb, gefitinib
|
|
mAb side effects:
|
infusion related: fever, chills, rigor, hypotension
allergic reaction: urticaria, SOB, angioedema, bronchoconstriction |
|
cetuximab MOA and types of cancer
|
human chimeric antibody
stimulates receptor internalization of EGFR and inhibits activation of EGRF head and neck cancer metastatic colon cancer |
|
cetuximab AE
|
hypersensitivity rxn (urticaria, bronchospasm, hypotension)
rash (grade 3-4) N/V/D |
|
panitumumab MOA and types of cancer
|
humanized antibody = HUGE ADVANTAGE of decreased AE
stimulates EGFR receptor interalization for pt that fail 5FU, irotcan or oxaliplatin chemo regimens metastatic colorectal cancer |
|
panitumumab AE:
|
grade 3 or 4 acne form rash
diarrhea, abdominal pain electrolyte depletion |
|
erlotinib MOA, cancers, and AE
|
targets kinase domain of EGFR and doesn't allow crossphosphorylation of the receptors
advanced nonsmall cell lung cancer as monotherapy combination therapy for advanced pancreatic cancer AE: diarrhea, rash |
|
her2/neu target therapy
|
trasuzumab, lapatinib
all normal epithelial cells contain 2 copies of HER2 cancer caused by increase in HER2 receptors homo- and hetero-dimerization = activation and signal cascade |
|
trastuzumab MOA and cancers
|
recombinant humanized mAb
binds to extracellular domain of HER2 and inhibits dimerization and internalization breast cancer **black box warning = can cause cardiomyopathy |
|
lapatinib MOA and cancers and AE
|
multikinase inhibitor of HER2 and EGFR
for metastatic breast cancer AE: diarrhea, hand and foot syndrome, nausea, rash, vomiting, and fatigue |
|
bevacizumab MOA and cancers
|
humanized mAb to VEGF
binds VEGF and inhibits its binding to VEGFR = inhibits , endothelial cell proliferation, invasion, migration, and survival. metastatic colorectal cancer, NSCLC, metastatic breast cancer, meastatic renal cell carcinoma (RCC), glioblastoma (GBM) |
|
bevacizumab AE
|
***blackbox warning for GI perforation
hypertension, arterial thrombotic events, proteinuria, surgery and wound healing complications, hemorrhage |
|
sunitinib MOA and cancers
|
multikinase inhibitor of VEGFR2, PDGFR, cKit, FGFR
Inhibits angiogenesis and cell proliferation Gastrointestinal stromal tumor (GIST) after failure of imatinib metastatic renal cell carcinoma |
|
sorafenib MOA and cancers
|
Multikinase inhibitor that targets Raf, MAPK, VEGFR2, PDGFR
Anti-proliferation and -angiogenesis by dual inhibition of the raf kinase pathway and the VEGFR pathways Metastatic renal cell carcinoma Liver cancer |
|
sorafenib AE
|
fatigue, weight loss, rash/ desquamation, hand-foot skin reaction, alopecia, diarrhea, anorexia, nausea and abdominal pain.
|
|
chronic myelogenous leukemia (CML)
|
starts in bone marrow and spreads to spleen and liver
philadelphia chromosome BCR-ABLE genes = CML chronic phase (CP), accelerated phase (AP) and blast crisis (BC), leading to metastasis and organ failure (lung, liver, spleen). |
|
bevacizumab AE
|
***blackbox warning for GI perforation
hypertension, arterial thrombotic events, proteinuria, surgery and wound healing complications, hemorrhage |
|
sunitinib MOA and cancers
|
multikinase inhibitor of VEGFR2, PDGFR, cKit, FGFR
Inhibits angiogenesis and cell proliferation Gastrointestinal stromal tumor (GIST) after failure of imatinib metastatic renal cell carcinoma |
|
sorafenib MOA and cancers
|
Multikinase inhibitor that targets Raf, MAPK, VEGFR2, PDGFR
Anti-proliferation and -angiogenesis by dual inhibition of the raf kinase pathway and the VEGFR pathways Metastatic renal cell carcinoma Liver cancer |
|
sorafenib AE
|
fatigue, weight loss, rash/ desquamation, hand-foot skin reaction, alopecia, diarrhea, anorexia, nausea and abdominal pain.
|
|
chronic myelogenous leukemia (CML)
|
starts in bone marrow and spreads to spleen and liver
philadelphia chromosome chronic phase (CP), accelerated phase (AP) and blast crisis (BC), leading to metastasis and organ failure (lung, liver, spleen). |
|
imatinib (1st gen) MOA
|
for CML
inhibits BCR-ABL and other TK's do not take other drugs with imatinib!!n binds to ATP binding pocket of kinase domain and inhibit tyrosine phosphorylation |
|
imatinib AE
|
myelosuppression, edema and fluid retention, severe congestive heart failure, GI bleeding, hypothyroidism, GI proliferation, renal + liver + cardiac toxicities in long term
|
|
nilotinib (2nd gen) MOA and AE
|
BCR-ABL receptor antagonists for those resistant to imatinib. CML.
AE: rash, elevated LFT, hyperglycemia, hypercholsterolemia, HA |
|
desatinib (2nd gen) MOA and AE
|
BCR-ABL receptor antagonists for those resistant to imatinib
AE: N/V/D, GI bleeding, edema/fluid retention, fatigue, HA, rash |
|
alemtuzumab MOA and cancer?
|
humanized Ab
binds to CD52 on T and B cells, tonsils, thymocytes, monocytes, macrophages. induced apoptosis for b-cell chronic lymphocytic leukemia |
|
rituximab MOA and AE
|
chimeric antibody
binds to cd20 on b cell lymphoycytes and non-hodgkin lymphoma AE: infection, thrombocytopenia,lung toxicity, dyspnea |