Term
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Definition
| Cell cycle specific: No. MOA: covalent modification of DNA. Resistance: Increased repair (and many others). Class or niche toxicity: myelosuppression, GI, and vesicle formation. |
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Term
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Definition
Cell cycle specific: No. MOA: Covalent modification of DNA (cross linking of DNA strands). Resistance: Increased repair (and many others). Class or niche toxicity: Myelosuppression,
GI, and
Vesicle formation |
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Term
|
Definition
Cell cycle specific: No. MOA: Covalent modification of DNA (cross linking of DNA strands). Resistance: Increased repair (and many others). Class or niche toxicity: Hemorraghagic cystitis (caused by acrolein) and Myelosuppression,
GI, and
Vesicle formation. Activated by CYP enzymes. Prevent cystitis with MESNA. |
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Term
| Nitrosoureas (Carmustine) |
|
Definition
| Cell cycle specific: No. MOA: covalent modification of DNA. Toxicity: myelosuppression, Cross the BBB. Treat brain tumors. |
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Term
|
Definition
Cell cycle specific: No. Binds to DNA and proteins. Toxicity: Nephrotoxicity, ototoxicity, peripheral neuropathy, and
Myelosuppression. Treats testicular cancer. |
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Term
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Definition
| Anti-folate. Cell cycle specific: Yes. MOA: Interferes with dihydrofolate reductase; thymidylate synthase no longer has substrate; inhibits DNA synthesis. Resistance: Gene amplification for DHFR. Toxicity: myelosuppression. Penetrates third space fluids; can me given intra-thecally . Toxicity managed by leucovorin (folinic acid which can be made into tetrahydrofolate in the absence of DHFR) |
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Term
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Definition
| Pyrimidine analog. Cell cycle specific: yes. MOA: Inhibits DNA and RNA synthesis by inhibiting thymidylate synthase. Toxicity: myelosuppression. |
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Term
|
Definition
| Purine analog. Cell cycle specific: Yes. MOA: Interferes with several steps in purine synthesis. Toxicity: myelosuppression. Activated by HGPRT; first pass metabolism by xanthine oxidase |
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Term
|
Definition
Antitumor antibiotic. Cell cycle specific: yes and no. MOA: Catalyzes the generation of reactive oxygen species which go on to damage DNA. Intercalates between DNA molecules and generates local reactive oxygen molecules (free radicals). Toxicity: Cardiotoxicity (delayed and cumulative)
Myelosuppression and
mucositis. Activated by CYP enzymes |
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Term
|
Definition
Antitumor antibiotic. Cell cycle specific: yes and no. Activated complex causes free radicals that cause DNA damage. Toxicity: Minimal myelosuppression;
Lung toxicity (restriction) |
|
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Term
| Vinblastine (vinca alkaloid) |
|
Definition
Cell cycle specific: yes. MOA: bind to the end of microtubules and cause depolymerization of microtubules. Toxicity: Myelosuppression and
SIADH. Long elimination phase (because it binds to tubules) |
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Term
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Definition
Cell cycle specific: Yes. MOA: taxol causes stabilization of tubules and blocks chromatin separation. Toxicity: Myelosuppression and
Hypersensitivity to the formulation in which it is given. Treats breast cancer. |
|
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Term
|
Definition
| Cell cycle specific: Yes. MOA: Binds to topoisomerase leading to ability to break the DNA but no repair mechanism. Toxicity: myelosuppression. |
|
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Term
|
Definition
Cell cycle specific: Yes. MOA: Binds to topoisomerase I (which is often overexpressed in tumors). Toxicity: Myelosuppression and
diarrhea |
|
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Term
|
Definition
Cell cycle specific: no. MOA: Competitive estrogen receptor antagonist (block signal for proliferation). Toxicity: Hot flashes and
Agonist in some tissues (partial agonist in other tissues). Treats ER + breast cancers |
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Term
|
Definition
| Cell cycle specific: MOA: Anti-tumor antibody against HER2 (epidermal growth factor) blocks ligand binding and down regulation of receptor itself on the surface (fewer receptors on the surface). |
|
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Term
|
Definition
| Cell cycle specific: No. MOA: Genotype specific therapy, binds to the ATP binding site of a very specific tyrosine kinase (Bcr-Abl) which is only found in those cancer cells. Resistance: emerging resistance. Treats CML. |
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