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128 Cards in this Set
- Front
- Back
what term means new growth
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neoplasia
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what is a neoplasm and what are its characteristics
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tumor; benign or malignant
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malignant tumors are characterized by what
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local invasion and distant metastasis
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what shows evidence of dedifferentiation
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malignant cells
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malignant cells show evidence of what
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dedifferentiation
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Cells that have undergone malignant transformation express signs of what
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immaturity such as the expression of fetal antigens
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what might show chromosomal abnormalities, and have altered metabolic pathways
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neoplasia
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A normal cell turns into a cancer cell because of ?
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one or more mutations in its DNA which can be inherited or acquired
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what happens during the formation of cancer cells
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Activation of proto-oncogenes to oncogenes; Inactivation of tumor suppressor genes
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what are the characteristics of cancer cells
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Dedifferentiation
Uncontrolled proliferation Invasiveness The ability to metastasize similar to normal cells/difficult to find areas of selective toxicity |
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what is significant about the proliferation of cancer cells
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not that it proliferates faster than normal cells but that it is unregulated
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what is apoptosis
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programmed cell death
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what is a hallmark of cancer cells
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resistance to apoptosis
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true or false cancer cells show telomerase expression
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true
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what is the significance of telomerase expression in cancer cells
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it repairs telomeres; allows cancer cells to continue to proliferate
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The multiplication of normal cells involves what
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division of the stem cells in a particular tissue to give rise to daughter cells
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daughter cells differentiate to become what
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mature cells
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what cells show a reverse process
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cancer cells
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what cancers have faster growth and a worse prognosis
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poorly differentiated cancers
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Normal cells are not found where
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outside designated tissues of origin
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Cancer cells will proliferate where and how
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wherever they reside and secrete enzymes that break down the extracellular matrix
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what are Metastases
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secondary tumors that are released from the primary tumor
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what are the principle cause of morbidity and mortality
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metastases
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what is a carcinogen
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any physical, chemical, or biological factor that causes or promotes cancer.
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what are examples of carcinogens
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Chemicals, radiation, and viruses
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what are oncogenes
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genes that are responsible for the conversion of normal cells into cancer cells.
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what are tumor suppressor genes
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genes that inhibit the transformation of normal cells into malignant cells
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Damage to the p53 tumor suppressor gene is associated with what
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cancers of the breast, lung, brain, colon, and bone
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what is associated with cancers of the breast, lung, brain, colon, and bone
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Damage to the p53 tumor suppressor gene
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Cancer chemotherapy is based on what
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principle of selective toxicity
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when treating cancer what is cell cycle specific
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anticancer agent that acts selectively on tumor stem cells when they are traversing the cell cycle and not when they are in the G-0 or resting phase
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when treating cancer what is cell cycle nonspecific
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anticancer agent that acts on tumor stem cells when they are traversing the cell cycle and when they are in the resting phase
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what is the log kill hypothesis
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concept used in cancer chemotherapy to mean that anticancer drugs kill a fixed proportion of a tumor cell population, not a fixed number of tumor cells
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what is an example of the log kill hypothesis
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a 1-log-kill will decrease a tumor cell population by one order of magnitude
i.e. 90% of the cells will be eradicated |
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what is growth fraction
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proportion of cells in a tumor population that are actively dividing
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what is the rescue therapy
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administration of endogenous metabolites to counteract the effects of anti-cancer drugs on normal cells
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what is the mech. of action of CCNS drugs (alkylating agents)
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They form reactive molecular species that alkylate nucleophillic groups on DNA bases, particularly the N-7 position of guanine.
This leads to cross-linking of bases, abnormal base pairing, and strand breakage |
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Tumor resistance to alkylating agents occurs through ?
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increased DNA repair, decreased drug permeability, or the production of trapping agents such as thiols
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thiols containt what
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a sulfur-hydrogen bond and are very nucleophillic
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what contains a sulfur-hydrogen bond and are very nucleophillic
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thiols
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what are the pharmacokinetics of Cyclophosphamide
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Hepatic transformation is needed for antitumor activity
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what is the clinical use of cyclophosphamide
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Non-Hodgkin’s lymphoma, breast and ovarian cancer, and neuroblastoma
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what toxicity is associated with cyclophosphamide
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GI distress, myelosuppression, alopecia, hemorrhagic cystitis, cardiac dysfunction, lung toxicity, and SIADH
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what are the pharmacokinetics of Carmustine (BCNU)
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High lipophilicity that facilitates CNS entry, used intravenously
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what is the clinical use of Carmustine (BCNU)
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Hodgkin’s disease, melanoma, multiple myeloma, brain cancer, mycosis fungoides
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what is the toxicity associated with Carmustine (BCNU)
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GI distress, myelosuppression, CNS dysfunction
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what are the pharmacokinetics of Cisplatin (Platinol)
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Used intravenously, widely distributed and cleared unchanged by the kidneys
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what is the clinical use of Cisplatin (Platinol)
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Testicular, bladder, ovary, uterine, head and neck cancers
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what is the toxicity associated with of Cisplatin (Platinol)
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GI distress, myelosuppression, neurotoxicity (peripheral neuropathy and acoustic nerve), renal damage
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what is the mech. of action of platinum analogs
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unclear but are thought to act in a similar fashion to the alkylating agents.
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are platinum analogs cell cycle specific or nonspecific
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nonspecific
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antimetabolites are structurally similar to what
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endogenous compounds
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antimetabolites are antagonists of what
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folic acid (methotrexate), purines (mercaptopurine), or pyrimidines (fluorouracil).
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are antimetabolites cell cycle specific or nonspecific
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specific
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when do antimetabolites primarily act
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in the S phase
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true or false: antimetabolites have immunosuppressant action
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true
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what drugs are the antimeabolites
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methotrexate, Mercaptopurine (6-MP), Fluorouracil (5-FU),
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what class of drug is methotrexate
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antimetabolite
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what is the mech of action of methotrexate
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Substrate for and inhibitor of dihydrofolate reductase.
This interferes with nucleic acid and protein synthesis. Tumor cell resistance mechanisms include decreased drug accumulation, changes in dihydrofolate reductase, and decreased formation of cytotoxic metabolites of methotrexate |
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what are the pharmacokinetics of methotrexate
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Both oral and IV administration afford good tissue distribution except to the CNS.
Excreted unchanged by the kidneys. Adequate hydration is required to prevent crystallization in renal tubules |
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what is the clinical use of methotrexate
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Acute lymphoblastic leukemia, choriocarcinoma, head and neck cancer, testicular cancer, osteogenic sarcoma, rheumatoid arthritis, psoriasis, and it is also used as an abortifacient
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what is the mech. of action of Mercaptopurine (6-MP)
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Purine antimetabolite which is activated by hypoxanthine-guanine phospho-ribosyltranferases (HGPRTases) to toxic nucleotides that inhibit several enzymes involved in purine metabolism.
A Prodrug |
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what is the resistance associated with mercaptopurine
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decreased activity of HGPRTase, or increased inactivation of the toxic nucleotide
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what are the pharmacokinetics of mercaptopurine
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Low oral bioavailability due to first pass metabolism.
The metabolism of mercaptopurine is inhibited by allopurinol |
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what is the clinical use of mercaptopurine
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Childhood acute leukemia
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what is the toxicity associated with mercaptopurine
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Bone marrow suppression, and hepatic dysfunction
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what is the mech of action of flurouracil
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Transformed to 5-FdUMP which inhibits thymidylate synthase and leads to “thymineless” death of cells
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what is the resistance associated with fluorouracil
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Decreased activation of 5-FU, increased thymidylate synthase activity, and reduced drug sensitivity of this enzyme
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what are the pharmacokinetics of fluorouracil
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Given IV and widely distributed including the CSF. Elimination is by metabolism
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what is the clinical use of fluorouracil
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Breast, colon, rectum, stomach, and pancreas, topically used for skin cancer
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what is the toxicity associated with lfuorouracil
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GI distress, myelosuppression, and alopecia
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what drugs are the antitumor antibioltics
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Doxorubicin (Adriamycin),
Bleomycin |
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what class is doxorubicin
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antitumor anitbiotics
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what class is bleomycin
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antitumor antibiotics
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what class is mercaptopurine
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antimetabolite
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what class is fluorouracil
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antimetabolite
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what is the mech of action of doxorubicin
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An anthracycline which can intercalate between base pairs, inhibit topoisomerase II, and generate free radicals.
Blocks the synthesis of RNA and DNA and causes DNA strand scission |
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is doxorubicin cell cycle secific or nonspecific
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nonspecific
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what are the pharmacokinetics of doxorubicin
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Must be given IV.
Metabolized in the liver and excreted in the urine, imparting to it a red color |
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wjhat is the clinical use of doxorubicin
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Lymphoma, sarcoma, acute leukemia, breast, lung, testes, thyroid, and ovary
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what is the toxicity associated with doxorubicin
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Myelosuppression, GI distress, and alopecia.
Unique side effect is cardiotoxicity |
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how does bleomycin act
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by binding to DNA, which results in single-strand and double-strand breaks following free radical formation, and inhibition of DNA biosynthesis
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is bleomycin cell cycle specific or nonspecific
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specific
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what drug causes accumulation of cells in the G2 phase of the cell cycle
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bleomycin
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what does bleomycin cause
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accumulation of cells in the G2 phase of the cell cycle
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what is the clinical use of bleomycin
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Hodgkin's and non-Hodgkin's lymphomas, germ cell tumor, head and neck cancer, and squamous cell cancer of the skin, cervix, and vulva
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what is the toxicity associated with bleomycin
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Pulmonary toxicity
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true or false: pulmonary toxicity is dose limiting
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true
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pulmonary toxicity usually presents as what
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pneumonitis with cough, dyspnea, dry inspiratory crackles on physical examination, and infiltrates on chest x-ray
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when is the incidence of pulmonary toxicity increased
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in patients older than 70 years of age, in those who receive cumulative doses greater than 400 units, in those with underlying pulmonary disease, and in those who have received prior mediastinal or chest irradiation
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are plant alkaloids cell cycle specific or nonspecific
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specific
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what are the plant alkaloids
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the vinca alkaloids, the podophyllotoxins, and the taxenes
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what class is Vincristine (Oncovin)
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plant alkaloid
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what is the mech of action of Vincristine (Oncovin)
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A spindle poison derived from the periwinkle plant.
Prevents the assembly of tubulin dimers into microtubules, and blocks the formation of the mitotic spindle. Acts on the M phase of the cell cycle |
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what is the resistance associated with Vincristine (Oncovin)
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occurs as a result of increased efflux from the cell by a transporter molecule
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what are the pharmacokintecis of Vincristine (Oncovin)
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Given IV. Good tissue penetration except into the CSF.
Cleared mainly by biliary excretion |
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what is the clinical use of Vincristine (Oncovin)
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Lymphoma, Hodgkin’s disease, Wilm’s tumor, childhood acute leukemia
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what is the toxicity associated with Vincristine (Oncovin)
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GI distress, alopecia, and myelosuppression.
Also causes peripheral neuropathy |
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what class of etoposide
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plant alkaloid
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what is etoposide
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podophyllotoxin derived from the May apple plant
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what is the mech of action of etoposide
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Interacts with Topoisomerase II to increase the degradation of DNA. Most active in the late S and early G2 phases
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what are the pharmacokinetics of etoposide
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Good oral absorption, eliminated via the kidney
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what is the toxicity associated with etoposide
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GI, alopecia, and myelosuppression
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what is the clinical use of etoposide
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germ cell cancers, small cell and non-small cell lung cancers, Hodgkin’s and non-Hodgkin’s lymphomas, and gastric cancer
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what class is Paclitaxel (Taxol)
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plant alkaloid
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what is Paclitaxel (Taxol)
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A taxane derived from the Pacific yew tree
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what is the mech of action of Paclitaxel (Taxol)
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A spindle poison which prevents microtubule disassembly into tubulin monomers
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what are the pharmacokinetics of Paclitaxel (Taxol)
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given IV
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what is the clinical use of Paclitaxel (Taxol)
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Breast and ovarian cancer
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what is the toxicity associated with Paclitaxel (Taxol)
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Myelosuppression, neuropathy, and hypersensitivity reactions
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what is prednisone used to treat
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acute leukemia, Hodgkin’s disease, and lymphoma
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what class is prednisone
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hormone
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what class is Diethylstilbestrol (DES)
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hormone
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what is Diethylstilbestrol (DES) used to treat
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prostate and breast cancer
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what are SERM’s
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mixed estrogen agonists that act as antagonists in certain tissues
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what class isTamoxifen
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hormone
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how does Tamoxifen act
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as an antagonist in hormone-responsive breast cancers where it prevents receptor activation by endogenous estrogen
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what drug has more agonist than antagonist action on bone and thus helps to prevent osteoporosis.
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tamoxifen
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what drug is a Selective Estrogen Receptor Modifier (SERM) which blocks the binding of estrogen to receptors of estrogen-sensitive cancer cells in breast tissue
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Tamoxifen (Nolvadex
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what is the mech of action of Tamoxifen (Nolvadex
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a Selective Estrogen Receptor Modifier (SERM) which blocks the binding of estrogen to receptors of estrogen-sensitive cancer cells in breast tissue
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what is the clinical use of Tamoxifen (Nolvadex
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treatment of receptor-positive breast cancers and may help prevent cancer in high risk women
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what toxicity is seen with tamoxifen
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nausea, vomiting, hot flushes, vaginal bleeding, hypercalcemia, and peripheral edema
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what drugs are biologic response modifiers
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interferon alfa-2,
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interferon alfa-2 is made by what
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lymphocytes
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what is the mech of action of interferon alfa-2
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inhibits cell proliferation
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what is clinical use of interferon alfa-2
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treatment of hairy cell leukemia, Kaposi’s sarcoma, and hepatitis
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what is the toxicity associated with interferon alfa-2
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Causes flu-like symptoms, fatigue, depression, nausea, vomiting, and diarrhea
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what are the miscellaneous anticancer drugs
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imatinib, Cetuximab, vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR), Bevacizumab, Asparaginase (L-asparagine amidohydrolase)
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