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30 Cards in this Set
- Front
- Back
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What are the mutations that induce malignancy |
growth preference
ability to lay down blood vessels
the ability to affect stroma
derailed apoptosis
avoid immune detection |
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What are the molecular targets for cances |
CD 20 in lymphoma,
surface and hormone receptors on breast cancer... |
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What are some of the sytemic treatments of malignancy |
rituximab = lymphoma and breast cancers |
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What are the principles of chemotherapy |
more drugs usually better then less
use with non overlapping toxicity
use drugs with different mechanisms of action
need to balance toxicity and efficacy
better use for supportive care: anti ememtics growth factor support |
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Chemotherapy can be: |
neoadjuvant; to shrink tumor before surgergy or radiation
adjuvant; used after surgery or radiation ro timprove survival
multimodality; in combination with surgery and radiation
palliative to treat symptoms |
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What is the major roadblock to successful cancer chemotherapy |
RESISTANCE
mutation amplification and deletion of targets
drug transport out of the cell or decreased cell entry
expression of alternate receptors |
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How do most chemotherapeutics work |
usually work in the cell division and replication phase of the cell cycle; S phase or DNA specific phase or M phase anti microtubule drugs |
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What are the major categories of chemotherapy agents |
Alkylating agents
Antimetabolites
Natural products
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What are alklyating agents |
Alkylating agents = all have basic cholorethlyamino structure that bind phosphates on DNA leading to mispairing ring opening and crosslinking; ANTI DNA CYCLOPHOSPHAMIDE is very immunosuppresive because it can lead to cytopenias, leukemogenesis can result from damaged stem cells resulting in leukemia
Melphalan uses to treat multiple myelomas and is give oral or IV
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What are platinum drugs |
cisplatin..
result in positive charges molecules that bind to nucleophilic sites on DNA and causes cross links |
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How does cisplatin work |
very active in solid tumors
has unique toxicities; emetogenic, nephrotoxicity, neurotoxicity, magnesium and potassium loss |
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What is the deal with carboplatin |
similar spectrum of activity
more toxic to bone marrow but less toxic to kidnesy and neural |
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What are the anit metabolite classes |
anti-fols works in S phase
pyrimidine and purine analogs |
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What is 5FU |
use mostly in solid tumors of GI tract
FdUMP inhibits TS by gettting incorporated into DNA and RNA |
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What is cytosine arabinoside |
Ara-C
analog of 2 deoxycidine enters via nuceloside transporters and then converted to active form and then gets incorportated into DNA and blocks DNA polymerase
major drug for treatment of acute leukemia given as a continious infucsion for 7 days
used in bone marrow cancers |
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What are the microtubule damaging agnets |
works in the M phase and interferes with microtubules
vincristine (O in CHOB) and vinblastine bind to beta tubulin and prevents formation
taxanes bind to beta tubuline site and promotes formation but doesnt let them disassemble |
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What is vincristine |
one of the earliest drugs
most effective in fast growting cells
not toxic to bone marrow can cause peripheral neuropathy, VESICANT to tissues needs to be in blood vessels |
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what are anthracyclcines |
doxorubicine (H in chob)
complexes with topisomerase II and leads to apoptosis, generates free radicals which attack DNA and oxidizes bases
used in lyphomas and leukemias
very toxic to carido, dose related and can lead to congestive heart failure |
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What are the proteosome inhibitors |
Bortezomib
if proteosome is inhibited the IkappaB bound to NfKB can not destroy the ikappaB preventing NfKB from acting as a transcription factor that is used in survival proliferation adn anti apoptosis |
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What are the two large classes of targeted therapy |
Monoclonal Abs SURFACE EGFR, VEGF and CD receptors
Tyrosine kinase inhibitors INSIDE interfer with signal transduction |
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What are the tyrosine kinase inhibitors |
influence gene transcription and DNA syntheiss that in cancers often are mutated leading to a preferential env.
leads to uncontrolled growth or deranged cell death |
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What is the role of the VEGF receptor |
increased in tumor cells to allow for greater angiogenesis for tumors |
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What are the VEGF drugs |
bevacizumab = avastin, renal cell carcinoma lung cancer colorectal cancer, not used in hematologic cancers
Sorafenib or sunitinib both competivielt inhibit the binding of ATP to the TK domain on the VEGF receptor 2 |
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What are the class effects of VEGF drugs |
THINK RENAL vessel injury and bleeding
hypertension
proteinuria
aterial thromboembolic evnets |
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What are the EGFR drugs |
is a transmembrane receptor tyrosine kinase, common in your lining cancers
Monoclonal; cetuximab, pantimumab colon
tyrosine kinases inhibtors; erlotinib |
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What are the class side effects of EGFR drugs |
rash anorexia fatigue
trastuzumab side effects = cardiotoxicity in breat cancer |
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What are IMiDs |
immunomodulatory regulators
thalidomide, lenalidomide, pomalidomide
direct anti proliferative and pro apoptotic effect, interrupt cell interactions with adhesion molceules, inhibits IL6 and TNF production, enhanced NK and T cell mediated toxicity |
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What are the class effects of immunomodulatory regulators |
peripheral neuropathy
somnolence
bone marrow supression
birth defects |
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What is rituximab |
chimeric, anti-CD20, not on the late B cell
has dramatically changes the prognosis in patients with NHL
as well as uses in autoimmune disease |
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What are the side effects of rituximab |
infusion reactions
viral reactivation especially hepatitis B
immunosuppression
progressive multifocal leukoencephalopathy whihc is rare but possible |
