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50 Cards in this Set

  • Front
  • Back
Mechanism of Methotrexate
S phase specific; folic acid analog inhibits DHF reductase (decr dTMP and DNA/protein synth)
Clinical use of methotrexate
Leukemias, lymphomas, choriocarcinoma, sarcomas
Abortion, ectopics pregnancy, RA, psoriasis
Toxicity of methotrexate
Myelosuppression, reversible w/leucovirin
Macrovesicular fatty change in liver
Mechanism of 5-fluorouracil
S phase specific antimetabolite
Pyrimidine analo bioactivated by 5-F-dUMP which covalently complexes folic acid
This complex inhibits thymidylate synthase
Clinical use of 5FU
Colon cancer/other solid tumors
Basal cell carcinoma (topical)
Synergy with MTX
6-mercaptopurine (6-MP) mechanism
Blocks de novo purine synthesis; activated by HGPRTase
Clinical use of 6 mercaptopurine
Leukemias/lymphomas (not CLL or Hodgkins)
Toxicity of 6 mercaptopurine
Bone marrow, GI, liver
Metabolized by xanthine oxidase so incr toxicity with allopurinol
Mechanism of cytarabine
Inhibits DNA polymerase
Clinical use of cytarabine
AML, ALL, high grade NHL
Toxicity of cytarabine
Leukopenia, thrombocytopenia, megaloblastic anemia
Mechanism of cyclophosphamide, ifosfamide
Alkylating agents; covalently x link (interstrand) DNA at guanine N-7. Requires bioactivation by liver.
Clinical use of cyclophosphamide
Breast and ovarian carcinomas
Mechanism of nitrosoureas (carmustine, lomustine, semustine, streptozocin
Alkylate DNA
Require bioactivation
Cross BBB
Clinical use of nitrosoureas
Brain tumors (incl GBM)
Toxicity of nitrosoureas
CNS toxicity (dizziness, ataxia)
Cisplatin, carboplatin mechanism
Cross link DNA
Clinical use of cisplatin, carboplatin
Testicular, bladder, ovary, and lung carcinoma
Toxicity of cisplatin
Nephrotoxicity, acoustic nerve damage
Busulfan mechanism
Alkylates DNA
Clinical use of busulfan
Also ablate bone marrow in BMSCT patients
Toxicity of busulfan
Pulmonary fibrosis, hyperpigmentation
Doxorubicin, daunorubicin mechanism of action
Generate free radicals and noncovalently intercalate in DNA 9create breaks to decr replication)
Clinical use of doxorubicin
Part of ABVD combo for Hodgkin's
Solid tumors
Toxicity of doxorubicin
Marked alopecia
Dactinomycin mechanism
Intercalates in DNA
Clinical use of dactinomycin
Wilm's tumor
Ewing's sarcoma
Toxicity of dactinomycin
Mechanism of bleomycin
Induces formation of free radicals which cause breaks in DNA
Clinical use of bleomcin
Testicular cancer
Hodgkin's lymphoma
Toxicity of bleomycin
Pulmonary fibrosis
Skin changes
MINIMAL myelosuppression
Etoposide mechanism of action
G2 phase specific agent aht inhibits topoisomerase II and incr DNA degradation
Clinical use of etoposide
Small cell carcinoma of lung/prostate/testicular carcinoma
Toxicity of etoposide
Myelosuppression, GI irritation, alopecia
Prednisone mechanism of action
May trigger apoptosis
Clinical use of prednisone
Most commonly usedglucocorticoid used in cancer chemo
Used in CLL, hodgkin's (MOPP regimen)
Also used in autoimmune diseases
Mechanism of tamosifen, raloxifene
SERMs-receptor antagonists in breast, agonists in bone, block binding of estrogen to estrogen receptor positive cells
Clinical use of tamosifen, raloxifene
Breast cancer, also useful to prevent osteoperosis
Toxicity of tamoxifen, raloxifene
Tamoxifen may incr risk of endometrial carcinoma via partial agonist effects "hot flashes"
Trastuzumab mechanism
Monoclonal antibody against HER-2 helps kill breast cancer that overexpressed possibly due to antibody dependent cytotoxicyt
Clinical use of trastuzumab
Metastatic breast cancer
Mechanism of imatinib
Philadephila chromosome tyrosine kinase inhibitor
Clinical use of imatinib
GI stromal tumors
Toxicity of imatinib
Fluid retention
Mechanism of vincristine, vinblastin
M phase specific alkaloids that bind to tubulin and block polymerization of microtubules so that mitotic spindle cannot form
Clinical use of vincristine
MOPP regimen for Hodgkin's
Wilm's tumor
Toxicity of vincristine/vinblastine
Vincristine-neurotoxicity, paralytic ileus
Cinblastine does bone marrow suppression
Mechanism of palitaxel/other taxols
M phase specific
Bind to tubulin and hyperstabilizie polyerized tubules so that the mitotic spindle cannot break down (anaphase cannot occur)
Clinical use of paclitaxel
Ovarian and breast carcinoma
Toxicity of paclitaxel
Myelosuppression and hypersensitivity