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32 terms

antneoplastic chemotherapy

STUDY
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oncogenes
genes when mutated become constitutively active, and thus lead to cancer
*often involved in signal transduction pathways
tumor suppressors
genes when mutated become inactive, thus lead to cancer
*often involved in check point controls
minimum of four oncogenes or tumor suppressor genes must be mutated in the same cell
minimum of four oncogenes or tumor suppressor genes must be mutated in the same cell
selective toxicity
oncogenes: design drugs that prefer the mutated form

tumor suppressors: if we damage cancer cells, they won't have the mechanisms to stop and repair damage before progressing through cell cycle
class 1 agents
-exert effects on all cells both proliferating and on-proliferating
-kill both normal and malignant cells to same extent
class 2 agents
-cell cycle specific
-target proliferating cells in preference to resting cells
-will kill only cells in one specific phase of the cell cycle
class 3 agents
-cell cycle phase non-specific
-kill proliferating cells in preference to resting cell
key points of resistance
MOR: 1) mutation on target proteins which lower the affinity of the drug for its target
2) up-regulation of proteins which can counter the effects of chemotherapeutic drug

**consider the dosing schedule: given time off for normal cells to recover = ideal for resistance
antimetabolites/DNA synthesis inhibitors
-folate antagonists
-purine antagonists
-pyrimidine antagonists
-ribnucleotide reductase inhbitors
**affect cancer cells in S phase
methotrexate
-folate antagonist
MOA: inhibits DHFR
-class 2 (S phase)
Toxicitie:
-myelosupression
-mucositis
-renal failure
thioguanine
-purine antagonist
-MOA: class 2 (S)
-requires activation
-inhibts PRPP
5-fluorouracil
-pyrimidine antagonist
MOA: class 2 (S)
-requires bioactivation by THF
-**inhibits thymidylate synthase
-toxicities: myelosupression, hand-foot syndrome, cardiac symptoms of chest pain
hydroxyurea
-ribonucleotide reductase inhibitor
-DNA cannot be formed from RNA
DNA alkylating drugs
-MOA: class 3 (cell-cycle nonspecific)
-bind to DNA and cause cross-links
-includes mustard gas
leucovorin
-basically folic acid
-given if folate antagonist toxicities become too significant
topotecan
-blocks topoisomerase I from RELIGATING the DNA after single strand breakshave been made
etoposide
-allows topo II to create double strand breaks, but prevents unwinding, and thus religation
doxorubicin
-DNA intercalating drug
-MOA: fits into DNA grooves, some converted to free-radicals-causing single and double stranded DNA breaks
vincristine
-MOA: inhibits tubulin polymerization into microtubules
-toxicities: neurotoxic
paclitaxel
MOA: enhances polymerization and blocks depolymerization of microtubules
-toxicity: neurotoxic, hypersensitivity
rituximab
anti-CD20
trastuzumab
anti-HER2/neu
bevacizumab
anti-VEGF
panitumumab
anti EGF receptor
moa of monoclonal antibodies
1)opsonization
2)inhibition of function
3)for growth factor receptors - blockng of dimerization
imatinib
-tyrosine kinase inhibitor
-Bcr-abl
erlotinib
-tyrosine kinase inhibitor
-EGF receptor
bortezimid
MOA: inhibits 26S proteasome which is used to degrade proteins that have been ubiquinated
-toxicities: infusion reactions, neuropathies
inteferons
MOA: differentiation of tumor cells, changes in gene expression, changes in phosphorylation patterns
-Toxicities: flu-like symptoms
growth factors
MOA: stimulates growth of specific blood cells to help combat bone marrow suppression
*these drugs help with the adverse symptoms of chemo
tamoxifen
MOA: blocks binding of estrogen to estrogen receptor
toxicity: menapausal symptoms, masculinization
flutamide
MOA: inhibits bindng of testosterone to androgen receptor
toxicity: hot flashes, gynecomastia, nipple pain, glactorrhea, feminization, impotence