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cancer chemotherapy

cancer chemotherapy drugs

QuestionAnswer
CYCLOPHOSPAMIDE Nitrogen mustard
CYCLOPHOSPAMIDE MECHANISM Reactive carbon forms covalent bond with DNA Results in: DNA replication arrest DNA damage and chromosome breaks Mutagenic
CYCLOPHOSPAMID toxicity BONE MARROW TOXICITY- Most cause dose-limiting myelosuppression MUCOUSAL TOXICITY- Oral blister, intestinal denudation HAIR FOLLICLES- Hair loss NEUROTOXICITY- N/V, ALTERED MENTAL STATUS CARCINOGENIC MUTAGENIC
CARMOSTINE Nitrosourea
CARMOSTINE MECHANISM Reactive carbon forms covalent bond with DNA Nonenzymatic activation step Can cause G-C cross-links Highly lipid soluble (BCNU and CCNU)
CISPLATIN discription Platinum compounds No activated carbon moieties Spontaneous formation of reactive molecule Intra- and Inter-strand DNA cross-links
CISPLATIN Mechanism All enter cells via a Cu++ transporter CTR1 Are actively exported from the cell via Cu++ transporter ATP7A and ATP7B and by the multi-drug resistance protein 1 (MDR-1)
CISPLATIN toxicity Acute: N/V Delayed: nephrotoxicity, ototoxicity, peripheral neuropathy
CYTARABINE DEOXYCYTIDINE ANALOG
CYTARABINE MOA Mechanism: Biochemical pharmacology mirrors the uptake and metabolism of normal nucleosides Insertion into DNA stops cells cycle INDUCES APOPTOSIS
CYTARABINE Toxicity N/V, myelosuppression
5-FLUOROURACIL PYRIMIDINE ANALOGUES FLUOROPYRIMIDINES
FLUOROURACIL MOA Mechanism: Inhibits thymidine synthesis Covalently binds to thymidilate synthase Stops DNA synthesis Incorporates into RNA
FLUOROURACIL toxicity SEVERE N/V MYELOSUPPRESSION
MERCAPTOPURINE PURINE ANTAGONISTS 6-THIOPURINES
MERCAPTOPURINE Mechanism 6-MP: INHIBITS ADENOSINE AND GUANOSINE SYNTHESIS 6-TG: INHIBITS GUANOSINE SYNTHESIS
MERCAPTOPURINE Toxicity IMMUNOSUPPRESSION MYELOSUPPRESSION HEPATOTOXICITY
METHOTREXATE description and effects FOLIC ACID ANALOG Essential dietary factor Transformed enzymatically into FH4 Cofactor for methyl group transfer in synthesis of thymidine
METHOTREXATE Mechanism Inhibition of dihydrofolate reductase
METHOTREXATE Toxicity MYELOSUPPRESSION mucositis diarrhea RESCUE THERAPY: TOXICITY CAN BE REVERSED WITH L-LEUCOVORIN (REDUCED FOLATE)
VINCRISTINE VINCA ALKALOIDS ANTIMITOTICS: drugs that inhibit mitosis
VINCRISTINE Mechanism INHIBITION of microtubule POLYMERIZATION INHIBITS MITOSIS
VINCRISTINE Toxicity MYELOSUPPRESSION, HAIR LOSS, NEUROTOXICITY
TAXOL ANTIMITOTICS: drugs that inhibit mitosis TAXANE
TAXOL Mechanism ENHANCES microtubule POLYMERIZATION Metaphase arrest INHIBITS MITOSIS
ETOPISIDE EPIPODOPHYLOTOXINS TOPIOISOMERASE INHIBITORS
ETOPISIDE Mechanism Inhibits DNA TOPIOISOMERASE II Inhibits DNA TOPIOISOMERASE II BLOCK Cells in G2 and S-PHASE
ETOPISIDE Toxicity ACUTE: N/V , hypotension DELAYED: Myelosuppression, Hair Loss
TOPTECAN CAMPTOTHECINS TOPIOISOMERASE INHIBITORS
TOPTECAN Mechanism Inhibits DNA TOPIOISOMERASE I BLOCK Cells in G2 and S-PHASE
TOPTECAN Toxicity ACUTE: N/V DELAYED: Myelosuppression
DOXORUBACIN TOPIOISOMERASE INHIBITORS ANTITUMOR ANTIBIOTICS ANTHRACYCLINES
DOXORUBACIN Mechanism INHIBITION OF TOPIOSOMERASE II BINDING W/ DNA AND RNA RELEASE OF FREE RADICALS BINDING TO CELL MEMBRANES AND ALTERING FLUID/ION TRANSPORT
DOXORUBACIN Toxicity ACUTE: MYELOSUPPRESSION, NAUSEA, RED URINE DELAYED: CARDIOTOXICITY, MOST LIKELY DUE TO THE RELEASE OF FREE RADICALS RESULT IN Heart Failure
MITOMYCIN C Mechanism ANTITUMOR ANTIBIOTICS
MITOMYCIN C DOES NOT INHIBIT TOPIOISOMERASES Cross-links w/ DNA Forms free radicals, results in DNA damage
MITOMYCIN C Toxicity N/V DELAYED: MYELOSURESSION, ANOREXIA, HEMOLYSIS
IMATINIB Tyrosine and other Kinase Inhibitors
IMATINIB mechanism Stops the active kinase from binding to substrate therefore the malignant phenotype is not expressed
IMATINIB resistance 3 different POINT mutation in the kinase domain of ABL-B Prevents drug from binding
IMATINIB interactions Ketoconazole (inhibts Cyp3A4) increases half life Rifampin (induces Cyp3A4) decreases half life
ERLOTINIB EGFR Tyrosine Kinase inhibitors
ERLOTINIB Mechanism Competes with ATP-binding site
ERLOTINIB Resistance Mutation in kinase domain
CETUXIMAB Monoclonal Antibodies
CETUXIMAB mechanism monoclonal Ab to EGFR binding domain
CETUXIMAB Main Adverse Effects Diarrhea, acneiform rash, nail changes, headaches, possible anaphylactic reactions
BEVACIZUMAB Inhibitors of Angiogenesis HUMANIZED monoclonal Ab Vascular Endothelial Growth Factor-a (an isoform of VEGF-a
BEVACIZUMAB mechanism Delays progression of renal cancer, glioblastoma Available via infusions
BEVACIZUMAB Main Adverse Effects Excessive bleeding, dec wound healing, HT, proteinuria, thromboembolic events.
SORAFENIB Inhibitors of Angiogenesis COMPETITIVE inhibitors of ATP-binding site of VEGF-R2 Also effects activation of other RTKs (e.g. PDGF-Rβ)
SORAFENIB Main Adverse Effects Excessive bleeding Dec wound healing Hypertension Proteinuria Thromboembolic events
Created by: ksoul6
 

 



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