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44 Cards in this Set
- Front
- Back
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Define what Cell Cycle Specific means in terms of caner chemo drugs
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Cells must be mitotically active for drug to produce its effects
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Define what Cell cycle non-specific means in terms of cancer chemo drugs
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Drug effect may be enhanced but not dependent on mitotic activity
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Cell cycle specific drugs are effective for what types of tumors?
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high growth fraction malignancies
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Cell cycle non-specific drugs are effective for what types of tumors?
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High growth AND Low growth raction malignancies (as opposed to cell cycle specific drugs which only work against high growth fraction malignancies)
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What are some of the ways cancers become resistant to drugs?
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Dec. drug uptake/ Inc drug efflux
Dec. drug activation / Ine drug INactivation Over-expression or mutation of drug target Increased repair of drug damage to DNA Inc. nucleophile conc. of substances (=react with drugs like alkylating agents to keep them from working) |
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How do drugs become resistant to cancer meds via efflux?
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Cancer cells up-regulate p-glycoprotein or multi-drug resistance protein; Both are active transporters
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Whats the therapeutic index (median toxic dose / median effective dose) for most cancer drugs?
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1
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Whats the purpose of using allopurinol with cancer drugs?
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Allopurinol protects the kidneys from uric acid damage. uric acid is a product of nucleic acid breakdown, which is occuring at high levels when we give anticancer drugs = protects from uric acid crystal damage or renal stones
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How does allopurinol inhibit uric acid production?
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Allopurinol inhibits xanthine oxidase
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How do we administer most cytotoxic drugs?
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IV
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T/F: many anti-cancer drugs are actually mutagens, and can cause a cancer to spring up 10 or more years after they have been given
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TRUE
Esp. a problem after Alkylating agents are used. |
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What are some examples of some naturally fast-growing normal cells that are likely to be affected by anti-cancer drugs?
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Blood cells
digestive tract cells reproductive system cells Hair follicles (ie why cancer treatment pts are bald...) |
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How do Alkylating drugs (agents) work to stop cancer?
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Form highly reactive alkyl groups that COVALENTLY bind DNA
ie they alkylate DNA at guanine --> cross-linking --> replication arrest --> cell death |
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How do anti-metabolites -work to be anti-cancer?
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They resemble cancer metabolites --> Interfere with DNA synth
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Why do we combine two or more anti-neoplastic drugs when treating cancer?
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To hit the cancer harder. many cancers have evolved to be made up of many dif types of cells, so we hit them with drugs that target dif. steps in the cell cycle to get the maximum effect
Maximizes cell kill by using different attack mechanisms Decreases resistance development Decreases doses and toxicities |
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Whats the RULE in cancer therapy?
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combine 2 or more anti-cancer agents
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For Leukemia, define Induction
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Given to Induce remission
Commonly used in tx of ACUTE leukemias |
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Define remission
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Absence of disease in pt with chronic illness
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Whats the initial intensive round of tx given to a leukemia pt called?
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induction
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What does Induction usually achieve?
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A remission with no evidence of leukemia cells in the blood or bone marrow
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Whats the purpose of intensification in the tx of leukemia?
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to get rid of clinically UNDETECTABLE disease = a 2nd, 3r, or 4th intensive tx with chemi
Given to inc. chances of cure |
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Define maintenance in terms of leukemia tx
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Given to prevent relapse. Less intense doses of chemo are given over a long period of time
Aim = to kill any remaining leukemia cells |
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How is Antimicrobial tx given?
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Low, continuous dose (as opposed to anticancer chemo = high intermittent dose)
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How is Anticancer chemo given?
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High, intermittent dose
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Which has the higher selective toxicity: anti-microbial or anti-cancer drugs?
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Anti-microbial (b/c bact. cells are very dif than human cells)
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Why do anticancer drugs have a lower selective toxicity than anti-microbial drugs?
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Anti-caner drugs are less selective toxically b/c they have to be....cancer cells are very similar to human cells, thus selective tox is limited considerably by toxicity to normal cells
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What is considered a "cure" in anticancer therapy?
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Dissappearance of any evidence of tumor for several years and a high probability of normal life span.
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What is considered a clinically complete remission?
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Tumor size decreased to a size no longer detectable clinically
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What are some factors that affect response to chemo drugs?
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Host: health, immunocompetence, tumor size
Tumor: Growth fraction, tumor mass doubling time, total tumor burden, cell cycle phase, drug resistance |
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What are some tumor growth kinetics that affect sensitivity to chemo drug?
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Growth fraction
Doubling time tumor burden cell cycle phase drug resistance |
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T/F: Pure loagarithmic tumor growth is an exception, not the rule
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TRUE
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Define growth fraction
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Fraction of tumor that is growing ie cells are dividing / in the cell cycle
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What determines growth of solid tumors?
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Nutrient availability, Vascularization
Diffusion - limited growth, center may be necrotic |
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Tumor are more susceptible to cancer drugs with a 1. small growth fraction 2. large growth fraction
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LARGE
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T/F; The doubling time (time to double tumor) varies by cancer
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TRUE
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Tumors with an 1. Inc. 2. Dec doubling time are more susceptible to cancer drugs
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INC
(b/c drugs target cell division....the more time a cancer cell spends dividing, the more susceptible it will be to cancer drug) |
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Which are more sensitive to cancer drugs, small or large tumors?
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small tumors, b/c more cells are dividing
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Where is P-glycoprotein normally expressed?
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Certain secretory tissues
Capillary endothelial cells Brain |
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Where is Multi-drug-resistant protein usually expressed?
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Epi cells
Colon, Liver, Adrenal, Pancreas, Kidney |
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Therapeutic effects on the tumor and toxicity are normally ______=related
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DOSE-related
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How to Antibiotics work to tx cancer?
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Bind DNA or assoc. protein --> Inhibit RNA synth --> DNA strand breaks via free radical production or Inhibition of TOPO II
Overall: Inhibit Topo 1 or Topo 2 = DNA breaks |
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How do anti-metabolites work to tx cancer?
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They mimic cancer metabolites, and interfere with DNA synth or the synth of DNA precursors
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How do Anti-mitotics work to tx cancer?
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Disrupt chemo dynamics --> disrupt cellular stuff necessary for DNA replication and mitosis
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Whats the relationship between doubling time and cancer susceptibility to drug?
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faster doubling time = inc. susceptibilty
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