27 – Antineoplastics – Flashcards
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Overview of Antineoplastic Agents (picture)
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- all inhibit DNA synthesis in some way
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Characteristics of Cancer Cells
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- Uncontrolled proliferation - *Dedifferentiation with loss of function* - Invasiveness - Metastases
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The log-kill hypothesis (chart)
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dash line - have cancer, don't do anything about - symptoms - tx will prolong survival, but you will die younger - you MUST eradicate all cancer cells to get rid of the disease - surgery + radiation ; shorter tx time
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CHEMOTHERAPY
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- Primary treatment for hematologic and diffuse cancers eg leukemias - *Adjuvant chemotherapy* after surgery ; radiation of solid tumors - *Neoadjuvant chemotherapy* before surgery improves surgical results eg in osteogenic sarcoma / breast cancer (CA) to downstage tumor - *Chemoprotection* to prevent cancer in high risk individuals
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Concepts Related to Chemotherapy
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- Selective toxicity - Cell kinetics: cycle time, growth fraction - Cell cycle phases - Cell phase and cycle specificity for drug action - Cancer growth
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Cell cycle of cancer cell
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- most drugs work in S phase M phase: vincristine S + G2: etoposide G2: Bleomycin
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Cell cycle ; site of action of antineoplastic agents
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- cell cycle agents vs. non specific drugs (these have the MOST ADRs, aggressive)
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Common Toxicities
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- Bone marrow suppression (BMS), infections (blood cells divide everyday) - Damage to GI epithelium, ulcerations, mucositis, stomatitis - Skin damage / sores - Loss of hair (alopecia) - Sterility / teratogenicity / *carcinogenicity (mainly alkylators)* - cancer tax's that cause cancer - Nausea / vomiting (N/V)
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*Drug resistance*
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- Decreased permeation/* increased drug efflux via P-glycoprotein transporter* (e.g., *methotrexate and vincristine*) - Increased intracellular conc. of thiols - Increased activity of DNA repair pathways - Increased rates of metabolism
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Chemical structure of nitrogen mustards
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- cyclophosphamide, ifosfamide, + mechlorethamin are important
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Mechanism of action of alkylating agents
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- alkylating action that attaches to DNA; eventually will cause cell death which you want in cancer (example of *meclorethamine*)
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Meclorethamine: Clinical indication
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- Most commonly used as a component of the mechlorethamine, vincristine, prednisone, procarbazine (MOPP) regimen in Hodgkin's disease (nitrogen mustard - alkylating agent)
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Meclorethamine: Pharmacokinetics
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- IV, rapid action/short duration, spontaneously converts to reactive metabolite; potent vesicant, extravasation causes severe pain / necrosis - lots of pain at injection site (nitrogen mustard - alkylating agent)
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Meclorethamine: ADRs
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- Highly reactive, do not mix with any other drugs, decomposes within 30 minutes - Myelosuppression (BMS) dose-limiting; severe nausea/vomiting, alopecia (nitrogen mustard - alkylating agent)
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Cyclophosphamide: Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Broad-spectrum alkylator, PO / IV - Prodrug, activated by liver P-450 enzymes - Phosphoramide mustard - the alkylator - Use for lymphomas and lymphocytic leukemia, ovarian cancers and solid tumors in children - *Acrolein (cytotoxic) - hemorrhagic cystitis* - cause blood in urine - Predrug hydration use of mesna disulfide - Severe N/V, dose-limiting BMS, alopecia, mucocutaneous, cystitis, amenorrhea/ azoospermia
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Metabolism of cyclophosphamide
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- Prodrug, liver converts it to active aldophosphamide - phosphoramide mustard = alkylating agent
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Ifosfamide: Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Related to cyclophosphamide,~ uses/toxicity - Slower hepatic activation to ifosfamide mustard, need larger doses, more acrolein, - Dose-limiting toxicity *hemorrhagic cystitis*, mesna usu. mandatory - CNS toxicity, thought to be due to formation of chloracetaldehyde - decreased arousal, somnolence, coma, seizures ; death - Advantage: Less bone marrow suppression (BMS)
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Chlorambucil: Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Alkylator, PO adm, good bioavailability - Main use: chronic lymphocytic leukemia (CLL), and non-Hodgkin's lymphoma (NHL) - Usually well tolerated on daily basis - Lower toxicity on bone marrow and more easily reversed - N/V usually @ higher doses, amenorrhea/ azoospermia, sterility, secondary acute leukemias with prolonged use
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Chronic Myeloid Leukemia (CML)
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- Genetic defect in Phila chromosome that inc abn enzyme BCR-ABL causing *unregulated tyrosine kinase* >excessive production white blood cells (WBCs) - Bone marrow transplant only cure - *Busulfan* - sulfonate alkylator, decs mainly granulocytes; pulmonary fibrosis, skin pigmentation - *Imatinib mesylate* - small organic molecule that inhibits ABL portion of abnormal enzyme; mild side effects, allows pts to live relative comfort for years
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Nitrosoureas: Carmustine - Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Nitrosourea, highly lipid soluble *crosses BBB* - Nonenzymatic conversion to alkylator - Particularly indicated for CNS /GI tumors, meningeal leukemias, NHL, Hodgkin's disease - Drug is a vesicant (i.e., local irritation) - Minimal cross resistance with nitrogen mustard alkylators - Delayed bone marrow toxicity - (N-V), BMS, mucocutaneous, hepato- / renal toxicity, pulmonary fibrosis at higher doses
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*Cisplatin*: Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Platinum metal salt, acts as an alkylator - Intra strand cross-linking of double-stranded DNA - *Wide use in solid tumors; testicular, lung, ovarian, breast* (aggressive - pancreatic) - ;90% bound to plasma proteins, 25% is excreted by 24 hours, 45% by 5 days - Usually severe/persistent nausea/vomiting - Dose-limiting *nephrotoxicity* (renal tubular damage); use hydration / diuretics (mannitol); amifostine - Ototoxicity/high tone loss/tinnitus; *peripheral neuropathy* - BMS usually mild
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*Oxaliplatin*: Uses, ADRs
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- uses - colorectal, pancreatic cancers/combined w/5-FU and leucovorin (FOLFOX regimen); *BMS*, peripheral neuropathy, diarrhea
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Carboplatin
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- similar uses as cisplatin - less hydration is needed; more BMS, less nephrotoxic
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Chemical Structures of Anthracyclines
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- know doxorubin
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Anthracyclines: Doxorubicin - Mechanism of action/clinical indications, pharmacokinetics
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- Anthracycline antibiotic acts by DNA intercalation, inhibits topoisomerase II, free radical formation;DNA scissions,; a vesicant - Isolated from the soil microbe: Streptomyces - Widely used lymphomas, leukemias, and many solid tumors (e.g.,osteosarcomas, lung/testicular/ ovarian/ breast cancers), - Converted to active alcohol intermediate, drug is cleared by hepatic metabolism and biliary excretion
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Anthracyclines: Doxorubicin - ADRs
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- BMS dose-limiting, stomatitis, EKG changes, tachycardia / cardiac arrhythmias - *Chronic cumulative dose-dependent cardiomyopathy irreversible CHF*
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Anthracyclines: Doxorubicin - Administer this drug along with:
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- *Dexrazoxane- chelates Fe prevents iron-mediated free radical generation, used to reduce cardiotoxicity*
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Anthracyclines: Daunorubicin
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- used in acute myelocytic leukemia (AML), acute lymphoblastic leukemia (ALL), acute nonlymphocytic leukemia (ANLL) - synthetic
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Anthracyclines: Mitoxantrone
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- synthetic analog of doxorubicin, less cardiac toxicity, used ANLL, breast cancer, others
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Anthracyclines: Idarubicin
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- a semisynthetic derivative with similar uses as daunorubicin, AML/ALL, claim of less cardiotoxicity
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Bleomycin: Mechanism of action/clinical indications, pharmacokinetics
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- Glycopeptide antibiotic intercalator, binds Fe DNA to form free radicals that cause DNA strand breaks, a.k.a. scissions, Cell cycle G2 phase - Isolated from Streptococcus verticillus - Uses: Headneck, testicular, cervix, esophagus, lung, Hodgkin's NHL - Admin. I.V. or I.M./inj. into bladder (i.e., bladder cancer), T1/2: 3 hours, 70% is excreted in urine
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Bleomycin: ADRs
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- *Dose-related pulmonary pneumonitis* with progression to fibrosis (most serious toxic effect - life threatening); mucositis, hyperpigmentation (hands) - Minimal BMS
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Antimetabolites: Methotrexate (MTX) - Mechanism of action/clinical indications, pharmacokinetics
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- Binds with great affinity to dihydrofolate reductase, prevents activation of folic acid; requires transport into cells - Polyglutamated within cells, long t1/2 in liver/kidney (months); MTX elim. by renal mech.(t1/2 = 2/10 hrs.); *increased P-glycoprotein transporter in cancer cells leads to resistance - Wide use: ALL, NHL, choriocarcinoma, solid tumors; also Rheumatoid arthritis and psoriasis*
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Leucovorin
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- *Leucovorin "rescue"* (activated folate) adm with high dose MTX (weak acid), administered within 24-36 hr; ? dose if plasma MTX remains elevated; *nephrotoxicity* /alkalinize urine and hydrate person to minimize toxicity
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Antimetabolites: Methotrexate (MTX) - ADRs
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- *nephrotoxicity* - *BMS, GI tract/ulcers*, skin, hepatic/pulmonary fibrosis, teratogen - Drug interactions - highly plasma protein bound drugs can displace MTX to inc toxicity, e.g. warfarin, sulfonamides, tetracyclines; also drugs that compete for tubular secretion, e.g. pens, cephs or reduce renal blood flow, e.g. NSAIDS
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Methotrexate/mechanism of action
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- build up of methotrexate polyglutamase in cells is a major mechanism of inhibitions
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5 - Fluorouracil (5-FU)
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- Activated to FdUMP, complexes with tetrahydrofolate (FH4) to *irreversibly inhibit thymidylate synthetase "thymineless death" and synthesis of DNA*, methotrexate also enhances activation of 5-FU, adm IV due severe GI toxicity - *Catabolized by dihydropyrimidine dehydrogenase (DPD); 5% of CA patient are deficient leads to increased BMS.* - FUMP >Triphosphate into RNA and miscoding - Carcinomas : used mostly in solid tumors of GI (esp colon), bladder, breast, head and neck, skin (topical application) - Capecitabine, related drug forms 5-FU, adm. PO - *BMS*, GI mucositis stomatitis, *skin hyperpigmentation*
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5-fluorouracil/mechanism of action
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- don't need to know enzymes
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Mercaptopurine: Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Purine-related analog, forms fraudulent nucleotides that inhibits purine synthesis - Also forms fraudulent bases in DNA that lead to miscoding ; faulty translation - *Use: childhood acute leukemia* - Bioavailability- only 10-50%, metabolized by HGPRT to 6-thioinosinic acid (active metabolite) increased when combined with methotrexate - Typical toxicity: BMS (usually mild), n-v, GI ulcer, hyperuricemia, long term use associated with risk of hepatotoxicity - Drug interaction with *allopurinol Xanthine Oxidase*
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Cytarabine - mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Cytosine analog, activated to CTP, inhibits DNA polymerase, incorporated into DNA, is an S-phase specific antimetabolite - Very active for adult AML - 20% bioavailability due to cytidine deaminase in GI tract and liver - BMS, GI, neurotoxicity - Liposomal IT injection for lymphomatous meningitis; may cause seizures/altered mental states
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*Gemcitabine*
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- new analog of cytarabine, less toxicity; an influenza-like syndrome, mild BMS; used in *pancreatic*, ovarian, bladder ; lung cancers
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Alkylators vs Antimetabolites - Summary of effects and adverse reactions
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Alkylators: - CCNS - Damage preformed DNA - Action on rapid ; slow/G? proliferating cells - Greater ability to kill BM stem cells/ cause secondary lymphomas /leukemias - Greater mutagenic, teratogenic, carcinogenic potential Antimetabolites: - CCS (S phase) - interfere with synthesis new DNA - action just on rapidly proliferating cells
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Vincristine (plant derivative) - Mechanism of action/clinical indications and adverse effects
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- M phase drugs metaphase arrest, binds tubulin, prevents microtubule formation - *P-glycoprotein transporter is increased and leads to resistance dev. in cancer cells - Plant alkaloid derivative of Vinca rosea* - Indications ALL, *Hodgkins/NHL lymphomas*, Wilms tumor - Vesicant action with extravasation, alopecia common, BMS usu. mild - *Neurotoxicity* dose-dependent/limiting (paresthesias, areflexia, neuritis, paralytic ileus/constipation, muscle weakness)
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*Vinblastine*
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- dose-limiting toxicity *BMS* (leukopenia), vesicant action, GI; use testicular CA, lymphomas
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Vinorelbine
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- used in non-small cell lung cancer (NSCLC), less toxicity
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Topoisomerase Inhibitors - Mechanism of Action
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- Topoisomerase I breaks and reseals single-stranded DNA. Inhibited by camptothecin analogues: *irinotecan and topotecan*, S-phase specific drugs - Topoisomerase II breaks and reseals double-stranded DNA. Inhibited by podophyllotoxins: *etoposide and teniposide* , S-G2 phase action
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Camtothecin Analogues - Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Inhibits DNA topoisomerase I - Large lactone ring structure, adm IV, bioavailability 20-35% - *Irinotecan* - adm IV rapidly metabolized in liver to highly active SN-38 metabolite. - Main use recurrent colorectal CA with 5FU/leucovorin (FOLFIRI), and with cisplatin in advanced small-cell lung cancer - *Topotecan* - active against glioma, sarcoma, lung, ovarian CA - ADRs (both), BMS, N-V-diarrhea (severe with irinotecan), alopecia
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Podophyllotoxins - Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- *Etoposide (broad-spectrum use)* and Teniposide (primarily used in combination drug regimens for lung (small cell), prostate, and testicular carcinoma) - Inhibit topoisomerase II, forms complex with DNA that causes permanent DNA strand breakage, active in S / G2 phases; etoposide also can cause metaphase arrest - Bioavailability 50% after P.O. adm., excreted in urine - Common toxicities: BMS, N-V, alopecia, mucocutaneous/GI, hypotension when infused to rapidly, secondary leukemias (etoposide)
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Paclitaxel - Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Derived from pacific/European yew tree - *Acts in M phase, inc polymerization of mitotic spindle, blocks disassembly* - Advanced breast and ovarian CA , lung - Inactivated by hepatic metabolism, CYP enzymes (Taxanes) - *Neutropenia *(BMS), thrombocytopenia, *peripheral neuropath*y (myalgia/sensory disturbances) are dose-limiting toxicities;
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Docetaxel
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- paclitaxel analog, used advanced breast/ovarian CA, ADRs: neutropenia, neurotoxicity (Taxanes)
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L-Asparaginase - Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Enzyme derived originally from E. coli - Inhibition of protein synthesis - Some leukemic (ALL)/lymphoma cells lack asparagine synthetase and require asparagine as an essential amino acid - Asparaginase metabolizes asparagine to the inactive aspartic acid - Allergic /hypersensitivity rxs, hyperglycemia, bleeding, hepatotoxicity, pancreatitis
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Pegaspargase
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- modified form for patients sensitive to L-asparaginase - conjugated with polyethylene glycol (PEG)
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Hormonal agents - Summary of mechanism
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- Many tumors of reproductive organs possess receptors for sex and steroid hormones that regulate growth - Removal of endocrine gland (outdated) - Administer opposite sex hormone (generally outdated) - Hormonal antagonists to block receptors, this has become the preferred method - Glucocorticoids (agonists); *prednisone *- suppresses lymphocyte mitosis; used in lymphomas/leukemias
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Tamoxifen - Mechanism of action/clinical indications, pharmacokinetics and adverse effects
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- Blocks cytoplasmic estrogen receptors (anti-estrogenic) - Originally developed as oral contraceptive - Cytostatic action, not tidal *less toxic; - Primary indication for breast cancer in node+ postmenopausals, trials underway for chemoprevention in high risk women - Adverse effects similar to post-menopausal : hot flashes, menstrual irregularities/bleeding, n-v, risk of endometrial cancer/uterine agonist
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Toremifene:
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- new analog (of Tamoxifen) /advanced breast CA
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Aromatase Inhibitors
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(e.g., anastrozole): advanced breast cancer
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Signaling of estrogen
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- receptor are tyrosine kinase
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Table 1 Principal genetic alterations in breast cancer
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*erb B2*
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Oncogenes/Tumor suppressor genes and the cell cycle
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CDK inhibitors
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Aromatase inhibitors/chemical structures
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- *lestrozole + anastrozole*
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Aromatase Inhibitors - Specific Drugs ; Mechanisms of action
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- Aromatase - responsible for the conversion of androstenedione and testosterone to estrone and estradiol, respectively - *Letrozole* - Inhibits estrogen synthesis from androstenedione and testosterone - *Anastrozole* - similar to letrozole - Exemestane - steroid, irreversible inhibitor of aromatase
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Aromatase Inhibitors - clinical indications and adverse effects
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- Indicated for treatment advanced breast cancer postmenopausal women with disease progression following tamoxifen therapy - ADRs: fatigue, n-v/GI, headache, muscle pain, estrogen-deficiency symptoms - Drugs contraindicated in pregnancy
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Gonadotropin-Releasing Hormone Agonists: Mechanism of action and clinical indications
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- *Leuprolide *- Buserelin - Goserelin - Peptide analogs of LH-RH that initially stimulate hormone production, but *chronically *inhibit FSH / LH secretion, (pharmacologic castration) monthly IM injections - Decreases gonadal production of both estrogen and testosterone - Use: prostate cancer
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Androgen receptor antagonists/chemical structures
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*flutaminde*
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*Flutamide*
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(Antiandrogens) - androgen receptor blocker; non-steroidal; used in prostate cancer ; initial leuprolide therapy; side effects: diarrhea, nausea reversible liver abnormalities ? Interrupt negative feedback of testosterone to pituitary-hypothalamic axis - attenuating impotency and loss of libido
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Cyproterone
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(Antiandrogens) - steroidal inhibitor of androgen receptor; used to treat prostate cancer antiandrogen side effects: hot flushes, impotency/loss of libido, gynecomastia
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*Procarbazine and Dacarbazine*:
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- methylation of DNA thereby inhibiting DNA synthesis (these agents primarily used in drug regimens of Hodgkin's lymphoma; e.g., doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD)) and brain tumors
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Gefitinib
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- small molecule, binds epidermal growth factor receptor; use NSCLC (non-small cell non lung carcinoma)
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Erlotinib:
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- blocks epidermal growth factor receptor that instructs cells to grow/divide, use NSCLC
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Hydroxyurea:
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- inhibits DNA synthesis in S phase; used in CML, but largely replaced by imatinib; still used to treat sickle cell anemia
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Mitotane:
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- adrenal necrosis adrenal tumors
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*Trastuzumab*
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(Monoclonal Antibodies) - binds, blocks, down-regulates human epidermal growth factor receptor HER 2, *approved in breast tumors that over express HER 2 (~ 30% of cases)* - Serious hypersensitivity and pulmonary reactions have resulted in deaths - ADRs: chills, fever, mouth sores, cardiac disturbances/CHF WILL BE ON TEST
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*Bevacizumab *
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(Monoclonal Antibodies) - binds vascular endothelial growth factor, starves tumors of blood supply needed for growth, used in colorectal/lung cancer
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Rituximab
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(Monoclonal Antibodies) - murine antibody that binds CD20 receptor normal/malignant B lymphocytes, used in NHL, induces complement-mediated lysis, apoptosis; ADR: can cause serious infusion-rx, fever/chills/bronchospasm/angioedema
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Tositumomab
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(Monoclonal Antibodies) - anti-B-cell (binds CD20 receptor) lymphoma antibody conjugated to an iodine 131 isotope, NHL
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Alemtuzumab
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(Monoclonal Antibodies) - human antibody against CD52 antigen on B and T-cell lymphomas; used in CLL
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A 32-year-old woman underwent segmental mastectomy for a breast tumor of 3 cm diameter. Lymph node sampling revealed 2 involved nodes. She underwent postoperative treatment with antineoplastic drugs. The chemotherapy regimen was fluorouracil, doxorubicin, cyclophosphamide & vincristine. Six cycles 1 mo apart of this chemotherpy regimen were planned. Adjunctive drugs included tamoxifen because the tumor cells were hormone receptor positive. The chemotherapy undertaken by this patient caused acute hemorrhagic cystitis. Which drug was most likely responsible for this toxicity? A. Cyclophosphamide B. Doxorubicin C. Fluorouracil D. Tamoxifen E. Vincristine
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A. Cyclophosphamide
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Which of the following best describes the mechanism of anticancer action of cellular metabolites of fluorouracil? (A) Cross-linking of double-stranded DNA (B) Inhibition of DNA-dependent RNA synthesis (C) Interference with the activity of topoisomerase I (D) Irreversible inhibition of thymidylate synthase (E) Selective inhibition of DNA polymerases
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(D) Irreversible inhibition of thymidylate synthase
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After several cycles of chemotherapy, the patient was found to have a high resting pulse rate. A noninvasive radionuclide scan revealed evidence of cardiomyopathy. The drug that is most likely responsible for the cardiac toxicity is: A. Cyclophosphamide B. Doxorubicin C. Fluorouracil D. Tamoxifen E. Vincristine
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B. Doxorubicin If asked to reverse toxicity - know chelating agent
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Which of the following is a cell cycle specific anticancer drug that acts mainly in the M phase of the cell cycle? A. Bleomycin B. Cisplatin C. Etoposide D. Methotrexate E. Paclitaxel
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E. Paclitaxel
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An adult patient is being treated for acute leukemia with a combination of anticancer drugs that includes cyclophosphamide, mercaptopurine, methotrexate, vincristine and prednisone. The patient complains of "pins and needle" sensations in the extremities and muscle weakness. He is not able to execute a deep knee bend or get up out of a chair without using his arm muscles. If these problems are related to the chemotherapy, which of the following is the most likely causative agent? (A) Cyclophosphamide (B) Mercaptopurine (C) Methotrexate (D) Prednisone (E) Vincristine
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(E) Vincristine
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Which of the following is a drug that is used in combination therapy for testicular carcinoma and is also associated with nephrotoxicity? (A) Bleomycin (B) Cisplatin (C) Etoposide (D) Leuprolide (E) Vinblastine
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(B) Cisplatin
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A cancer cell that is resistant to the effects of both vincristine and methotrexate probably has developed that resistance as a result of (A) Changes in properties of a target enzyme (B) Decreased activity of an activating enzyme (C) Increase in expression of a P-glycoprotein transporter (D) Increase in proteins that are involved in DNA repair (E) Increase in production of drug-trapping molecules
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(C) Increase in expression of a P-glycoprotein transporter
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A 23-year-old man with Hodgkin's disease was treated unsuccessfully with the MOPP regimen (mechlorethamine, vincristine, prednisone, procarbazine). He subsequently underwent a successful course of therapy with the ABVD regimen (doxorubicin, bleomycin, vinblastine, dacarbazine) Which of the following classes of anticancer drugs used in the treatment of this patient is cell cycle specific (CCS) and is used in both the MOPP and ABVD regimens? (A) Alkylating agents (B) Antibiotics (C) Antimetabolites (D) Glucocorticoids (E) Plant alkaloids
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(E) Plant alkaloids (Vincristine ; vinblastine)
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During the second course of drug treatment (ABVD regimen), this patient developed dyspnea, a nonproductive cough, and intermittent fever, Chest x-ray film revealed pulmonary infiltration. If these problems are due to the anticancer drugs to which has been exposed, the most likely causative agent is (A) Bleomycin (B) Dacarbazine (C) Doxorubicin (D) Prednisone (E) Vinblastine
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(A) Bleomycin
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All of the following agents have been used in drug regimens for the treatment of breast carcinoma. Which one has specific activity in a subset of female breast cancers? (A) Flutamide (B) Doxorubicin (C) Fluorouracil (D) Methotrexate (E) Trastuzumab
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(E) Trastuzumab
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A 55-year-old man presents with increasing fatigue, 15-pound weight loss, and a microcytic anemia. Colonoscopy identifies a mass in the colon and biopsy reveals colon cancer. The mass is surgically removed and the patient receives FOLFOX regimen (5-FU, leucovorin and oxaliplatin) for his adjuvant therapy. After the first weekly cycle of the therapy, which of the following adverse effects are likely for the patient to experience? (A) Shortness of breath (B) Swelling of hands (C) Skin rash (D) Myelosuppression (E) Brain pain
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(D) Myelosuppression
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A 28-year-old woman presents with a 1-cm mass in the right supraclavicular fossa. Biopsy reveals nodular sclerosing Hodgkin's disease that is advanced. Which of the following drugs are useful in Hodgkin's lymphoma? (A) Paciltaxel (B) Methotrexate (C) 5-fluorouracil (D) Vincristine (E) Cisplatin
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Comes down to two - best choice: (D) Vincristine
