antneoplastic chemotherapy
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32 terms
Terms | Definitions |
|---|---|
 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 |
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