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34 Cards in this Set

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"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