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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


-folate antagonist
MOA: inhibits DHFR
-class 2 (S phase)
-renal failure


-purine antagonist
-MOA: class 2 (S)
-requires activation
-inhibts PRPP


-pyrimidine antagonist
MOA: class 2 (S)
-requires bioactivation by THF
-**inhibits thymidylate synthase
-toxicities: myelosupression, hand-foot syndrome, cardiac symptoms of chest pain


-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


-basically folic acid
-given if folate antagonist toxicities become too significant


-blocks topoisomerase I from RELIGATING the DNA after single strand breakshave been made


-allows topo II to create double strand breaks, but prevents unwinding, and thus religation


-DNA intercalating drug
-MOA: fits into DNA grooves, some converted to free-radicals-causing single and double stranded DNA breaks


-MOA: inhibits tubulin polymerization into microtubules
-toxicities: neurotoxic


MOA: enhances polymerization and blocks depolymerization of microtubules
-toxicity: neurotoxic, hypersensitivity








anti EGF receptor

moa of monoclonal antibodies

2)inhibition of function
3)for growth factor receptors - blockng of dimerization


-tyrosine kinase inhibitor


-tyrosine kinase inhibitor
-EGF receptor


MOA: inhibits 26S proteasome which is used to degrade proteins that have been ubiquinated
-toxicities: infusion reactions, neuropathies


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


MOA: blocks binding of estrogen to estrogen receptor
toxicity: menapausal symptoms, masculinization


MOA: inhibits bindng of testosterone to androgen receptor
toxicity: hot flashes, gynecomastia, nipple pain, glactorrhea, feminization, impotence

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