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Cancer and Immune System Pharmacology

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Question 1

While reviewing charts in a general medicine cl inic you see that a patient, 55-year-old and with no history of cancer at all, i s taking methotrexate (MTX). What i s the most l ikely condition for which this “anticancer drug” i s being given?

A	Asthma or emphysema
B	Hyperthyroidism
C	Hyperuricemia or cl inical gout
D	Myasthenia gravis
E	Rheumatoid arthritis or psoriasis

Question 1 Explanation:

The main uses of methotrexate (MTX) for conditions other than responsive cancers are management of rheumatoid arthritis (RA) and psoriasis that is usually not responsive to other drugs. Doses and dosage schedules differ from those typically used for cancers. MTX is one of many disease-modifying antirheumatic drugs (DMARDs), which are also called slow-acting antirheumatic drugs (SAARDs) because their onset of symptom relief is much slower than traditional NSAIDs (salicylates and other first-generation COX-1/-2 inhibitors, or secondgeneration/COX-2 inhibitors, ie, the “coxibs”). Nonetheless, although the onset is considered slow, meaningful symptom relief usually occurs with as little as 3 to 4 weeks of therapy—faster than most of the other DMARDs. Note that other DMARDs, of which there are many, have no cancer-related uses. All the potential side effects, adverse responses, and contraindications that apply to using MTX for cancer apply to the drug’s use for RA or psoriasis.

Question 2

A 47-year-old woman with choriocarcinoma i s treated with methotrexate (MTX), given at dosages that you believe may cause s ignificant host cell Which drug would you give to l imit the toxic effects of the drug on normal host cells?

A	Deferoxamine
B	Leucovorin
C	N-acetylcysteine
D	Penicillamine
E	Vitamin K

Question 2 Explanation:

This essential technique to reduce host cell toxicity in response to methotrexate (MTX) therapy is often referred to as leucovorin (folinic acid) rescue. Methotrexate, a folic acid analog/antimetabolite, can be curative for women with choriocarcinoma and is also useful for non-Hodgkin lymphomas and acute lymphocytic leukemias (ALLs) in children. The drug kills responsive cancer cells by inhibiting dihydrofolate, an enzyme necessary for forming tetrahydrofolic acid (FH4). The FH4, in turn, is critical for eventual synthesis of DNA, RNA, and proteins. Inhibition of thymidylate synthesis is probably the single most important consequence in the overall reaction scheme. Some cancer cells are resistant to MTX because they lack adequate mechanisms for transporting the drug intracellularly. These include some head and neck cancers and osteogenic sarcomas. In such cases we need to give very large doses of MTX to establish a high concentration gradient that essentially “drives” it into the cells. Unfortunately, normal host cells depend on folate metabolism, they take up MTX well, and they will be affected. To protect normal cells we administer leucovorin (also called citrovorum factor or folinic acid) right after giving the MTX. It is taken up by the normal cells, bypasses the block induced by the MTX, and so spares normal cell metabolism. The leucovorin does not spare cancer cells: just as they cannot take up MTX well, they cannot take up the rescue agent and save themselves from cytotoxicity. Leucovorin rescue is not done “automatically” in every case when MTX is given. When low MTX doses are used leucovorin may be withheld until and unless blood counts show evidence of MTX-induced bone marrow suppression. However, it is quite usually given along with MTX when MTX doses are very high (as in severe or MTX-resistant cases), and host toxicity is very probable. There is another important and growing use of MTX: as a disease-modifying or slow-acting antirheumatic drug (DMARD, SAARD, respectively). Owing to toxicity (see below) it had been relegated to second- or third-line therapy of severe and/or refractory rheumatoid arthritis. Now that we have a better appreciation of the drug’s toxicity, and how to recognize it earlier and minimize its occurrences, it is being used much more, earlier on in therapy, for rheumatoid arthritis that is “moderate” and likely to progress rapidly. The main adverse responses to MTX, regardless of the purpose for which it is given, include bone marrow suppression, pulmonary damage (infiltrates, fibrosis), stomatitis, and lesions elsewhere in the GI tract. High doses can be nephrotoxic (risk reduced by maintaining adequate hydration and alkalinizing the urine). MTX is also teratogenic. Recall that deferoxamine (a) is used to treat iron poisoning (it is an iron chelator). N-acetylcysteine (c) is mainly used either as a mucolytic (mucus-thinning) drug for certain pulmonary disorders (eg, COPD) or as an antidote for acetaminophen poisoning. Penicillamine (d) is mainly a copper chelator, used for copper poisoning or Wilson disease. Vitamin K (e) is used for deficiency states, for combating excessive effects of warfarin, or for managing bleeding disorders in newborns of mothers who have been taking certain drugs (eg, anticonvulsants such as phenytoin) during pregnancy

Question 3

You order vincristine, the prototype of the vinca alkaloids, to a patient with a tumor that i s l ikely to be responsive to this What i s the most l ikely adverse response to this drug?

A	Nephrotoxicity, renal dysfunction or failure
B	Neutropenia
C	Peripheral sensory and motor neuropathy
D	Pulmonary damage
E	Thrombocytopenia, bleeding

Question 3 Explanation:

Vincristine is one of relatively few cytotoxic anticancer drugs, which does not cause bone marrow suppression (and all the potential consequences of that) as its main toxicity. Rather, it causes neuropathies involving both sensory and motor nerves. Paresthesias are a common example of the former (hearing loss can also occur); muscle weakness and obtunded reflexes are examples of the latter. Important note: Vincristine differs from the other two vinca alkaloids, vinblastine and vinorelbine, which do cause bone marrow suppression (and not neuropathies) as their main dose-limiting toxicity.

Question 4

A cancer patient develops severe, i rreversible cardiomyopathy because the maximum l i fetime dose of an anticancer drug was exceeded. What drug was most l ikely responsible for this?

A	Asparaginase
B	Bleomycin
C	Cisplatin
D	Cyclophosphamide
E	Doxorubicin
F	Vincristine

Question 4 Explanation:

Doxorubicin, an antitumor antibiotic, is cardiotoxic, and the risk for and severity of cardiomyopathy is dose-related. (There is a maximum recommended lifetime [cumulative] dose for this drug, and if it is exceeded the risk of cardiac damage rises significantly.) Asparaginase (a), used only for acute lymphocytic leukemia, tends to cause mainly pancreatitis, hepatic dysfunction, and allergic/hypersensitivity reactions. The main organ-specific toxicity of bleomycin (b), also an antitumor antibiotic, is pulmonary damage that presents initially usually as pneumonitis. It occurs in about 1 of 10 patients treated with this drug. In some cases the pulmonary damage will progress to pulmonary fibrosis that is, of course, irreversible. Cisplatin’s (c) main dose-limiting toxicity is renal damage, which can be prevented somewhat by ensuring that the patient is adequately hydrated and producing adequate amounts of urine. Diuretics may be used as adjuncts. The goal is to minimize accumulation of the nephrotoxic drug in the renal tubules and urine. (A related drug, oxaliplatin, tends to cause peripheral sensory neuropathies and does so in most patients who receive this drug.) Cyclophosphamide (d) has no particular organ-specific toxicity. Rather, main manifestations of toxicity involve rapidly growing cells such as those in the bone marrow, intestinal tract mucosae, and hair follicles. Vincristine’s (f) major dose-limiting toxicity is peripheral nerve damage: motor, sensory, and in some cases autonomic. It probably arises in a manner related to the drug’s anticancer effect: inhibition of microtubular function—or, in the case of nerves, neurotubules—as a result of drug binding to tubulin.

Question 5

A patient with Wilms tumor i s receiving a chemotherapeutic agent that i s described as working by intercalating into DNA strands, and that i s efficacious regardless of which stage of the cell cycle the tumor cells are Which drug best fi ts this description?

A	Anastrozole
B	Cytarabine (cytosine arabinoside)
C	Doxorubicin
D	Fluorouracil.
E	Tamoxifen

Question 5 Explanation:

Anthracycline-type antitumor antibiotics (doxorubicin, daunorubicin, idarubicin, etc) intercalate between and eventually bind to DNA base pairs. This distortion of the DNA chains makes the DNA an unsuitable template for RNA polymerase, and ultimately RNA and protein synthesis is inhibited. Dactinomycin is phase-nonspecific. Anastrozole (a) is a relatively new aromatase inhibitor. This oral agent is used for postmenopausal women with early or advanced breastcancer. In postmenopausal women, the major source of estrogen (which supports growth and replication of estrogen-dependent tumors) is adrenal androgens. Those androgens are metabolized by aromatase to estrogens. As a result, anastrozole depletes estrogens and can arrest tumor cell growth. Cytarabine (b, also called cytosine arabinoside) is a pyrimidine analog (antimetabolite) that is metabolized to the active moiety, ara-CTP. The ara-CTP becomes incorporated into DNA, with the main ultimate effect being suppression of DNA synthesis. It is highly specific for cells in S-phase. Fluorouracil (d), also an antimetabolite, inhibits thymidylate synthetase through its active metabolite, 5-fluoro-2′-dexoyuridine-5′- monophosphate (FdUMP). It is not phase-specific, but its activity depends on cells not being in the G0 stage. Tamoxifen (e) is used for breast cancers. It blocks estrogen receptors on the breast cancer cells (for which the main physiologic agonist is estradiol). Recall that tamoxifen is classified as a selective estrogen receptor modifier (SERM). Although it blocks estrogen receptors on responsive breast cancer cells and is therapeutic for them, it acts as an estrogen receptor agonist in the uterus. Thus, one of the main risks of therapy with tamoxifen is endometrial hyperplasia that may lead to endometrial cancer. Because the drug acts as an estrogen receptor agonist in some tissues and an antagonist in others, risk-benefit ratios must be considered carefully. The beneficial effects in active breast carcinoma may outweigh the risks of inducing endometrial disease. However, the preventative use in the absence of breast cancer has a much lower benefit-torisk ratio.

Question 6

A 42-year-old woman i s diagnosed with metastatic breast You consider use of tamoxifen, toremifene, or fulvestrant. Why might fulvestrant be the best choice, all other factors being equal?

A	Exerts antiplatelet, rather than thrombotic, effects
B	Lacks ability to cause hot flashes or other disturbing s ide effects
C	Lower ri sk of causing endometrial cancer
D	Provides cl inical cure, rather than palliation, in all patients
E	Significantly improves mineral density in, strength of, long bones

Question 6 Explanation:

Fulvestrant is associated with a much lower risk of causing endometrial pathology, including cancer. It is a “pure” estrogen antagonist. That effect, in breast tissue, is what accounts for the drug’s beneficial effects in some patients with metastatic, estrogen-supported, breast cancer. In contrast, tamoxifen and toremifene are classified as selective estrogen receptor modifiers (SERMs). Although they block estrogen receptors in breast tissue (just as fulvestrant does), they also have estrogenic (agonist) activity in some other tissues, notably the uterus. There they can cause endometrial proliferation, hyperplasia, and (apparently) an increased risk of endometrial cancer. Because fulvestrant lacks estrogen agonist activity, it will not enhance bone mineralization nor favorably modify cholesterol profiles, as the SERMs tend to do. The SERMs slightly increase the risk of thromboembolism. Fulvestrant may too, but it also lacks any ability to prevent platelet aggregation or thromboembolism. Hot flashes are fairly common with any of these drugs.

Question 7

A patient with chronic myelogenous leukemia (CML) i s being treated with Which s ide effect or other s i tuation should you anticipate in response to imatinib therapy?

A	A high rate of therapeutic failure, and the need to switch to interferons α-2a and -2b
B	Hypotension and hypovolemia due to s ignificant drug-induced diuresis
C	Interactions with other drugs that depend on or affect the cytochrome P450 system
D	Significant toxicity to normal host cells due to profound inhibition of tyrosine kinase
E	Thrombocytosis, with a high ri sk of intravascular clotting

Question 7 Explanation:

One of several problems with imatinib therapy is that it is a substrate for, and rather powerful inhibitor of, several cytochromes (CYP3A4, 2C9, and 2D6) that are important for the metabolism of many other drugs— warfarin, theophylline, and many others—whose actions can be increased excessively if dosages are not adjusted accordingly. Conversely, imatinib is a target of interactions by this mechanism. Phenytoin, carbamazepine, barbiturates, and rifampin are examples of drugs that can induce imatinib metabolism and reduce the clinical response to it; and such drugs as azole antifungals and erythromycin can reduce imatinib’s clearance and increase the risk of toxicity. Because of the issue of drug interactions, a high frequency of adverse responses, limited use (see below), and even cost, imatinib is generally reserved for use after a trial of interferons has proven inadequate. The reverse—using imatinib first—usually isn’t done. Hypotension and hypovolemia (b) are not what one would expect with this drug. Rather, we see a rather high incidence of fluid retention that may not only affect blood pressure, but also cause such other problems as ascites, pericardial and pleural effusions, and possibly pulmonary edema. Likewise, thrombocytosis (e) is the opposite of what typically occurs: thrombocytopenia and bleeding problems, plus neutropenia and an increased risk of infection are fairly common. Recall that chronic myelogenous leukemia cells do synthesize an abnormal constitutively active tyrosine kinase (Bcr-Abl) that is involved in (abnormal) protein phosphorylation. It is that aberrant tyrosine kinase—not ones found in normal host cells—that is affected by the drug and that confers selectivity for the drug’s actions. Thus, tyrosine kinase inhibition does not seem to account for the adverse effects of this drug on host cells.

Question 8

As a rule, large (and older) solid tumors are more difficult to eradicate when chemotherapy i s Which tumor-based property explains best the reason for this chemotherapeutic l imitation?

A	Growth fraction s lows, more cells enter G0
B	Higher tumor blood flow washes away anticancer drugs faster
C	P-glycoprotein activity decreases as tumors get older
D	Their higher metabolic rate makes them less vulnerable to chemotherapeutic agents
E	Topoisomerase activity (ability to self-repair DNA strand damage) increases with tumor s i ze

Question 8 Explanation:

Gompertzian analysis (a plot of the log of the number of cancer cells in a tumor vs time) shows that after a tumor has reached a certain size, the rate of tumor growth (and “overall metabolic rate”) slows: lower growth fraction or, stated differently, the longer it takes for the tumor to double in size. This slowed growth is partially due to more cells entering the G0 (resting) phase of the cell cycle, where responsiveness to many chemotherapeutic agents is lower. (One reason for this is the sheer size of the tumor as related to blood flow and the delivery of nutrients that the rapidly dividing cells need. Reduced nutrient and oxygen delivery not only reduce cell replication, but also delivery of the chemotherapeutic agents. Therefore answer b is incorrect.) P-glycoprotein activity (c) does not necessarily decrease with time or tumor size. However, even if it did, that would predict increased responsiveness to most anticancer drugs, because it is P-glycoprotein that normally pumps drugs out of the cancer cell. Self-repair mechanisms, as by topoisomerase (e), is not a factor in explaining reduced vulnerability of very large tumors.

Question 9

A man has prostate cancer that will be treated with Which drug are you most l ikely to use adjunctively when starting chemotherapy?

A	An aromatase inhibitor (eg, anastrozole)
B	Flutamide
C	Prednisone or another potent glucocorticoid
D	Tamoxifen
E	Testosterone

Question 9 Explanation:

Flutamide, one of a small number of androgen receptor blockers used for managing prostate cancer, is used as an adjunct to leuprolide. Leuprolide acts like gonadotropin-releasing hormone (GnRH; or luteinizing hormone-releasing hormone). When leuprolide therapy is started, it stimulates release of interstitial cell-stimulating hormone from the pituitary, thereby increasing testosterone production and supporting tumor growth. It is only with continued exposure to leuprolide that GnRH receptors become desensitized, and the eventual inhibition of testosterone production (and, thereby, support of tumor growth) occurs. Flutamide, by blocking androgen receptors, prevents the potential worsening of the tumor in the early phase of leuprolide therapy when testosterone levels rise. Even when leuprolide’s pituitary-desensitizing effects occur, androgens that can support prostate tumor growth will come from the adrenal gland. Their effects, too, are blocked by the flutamide.

Question 10

As part of the treatment plan for a Hodgkin disease patient we have given Which phrase best describes the anticancer mechanism of action of this drug?

A	Alkylates DNA, causing cross-links between parallel DNA strands
B	Blocks microtubular assembly and mitosis during M-phase
C	Inhibits topoisomerase, preventing repair of DNA strand breaks
D	Intercalates in DNA strands, thereby preventing DNA replication by mRNA.
E	Stabilizes microtubular arrays, thereby preventing mitosis

Question 10 Explanation:

Mechlorethamine, like cyclophosphamide (and carmustine and several others), is an alkylating agent. They are called bifunctional alkylating agents because they can covalently bind to DNA in two places (“nucleophilic attack”), thereby forming cross-links between two adjacent strands or between two bases in one strand. This ultimately disrupts DNA and RNA synthesis or may cause strand breakage. Cyclophosphamide (which can be considered the prototype of the alkylating agents) is actually a prodrug —it requires metabolic activation in order for its effects to occur. Cyclophosphamides (and other alkylating agents) are cell cycle-nonspecific, although their efficacy is greater when cells are not in G0. Bleomycin, dactinomycin, and doxorubicin are good examples of drugs that intercalate in DNA strands (d). Thus, the altered DNA no longer serves as an adequately precise template for eventual synthesis of more functional DNA and RNA. They are classified as antitumor antibiotics. Etoposide and topotecan are examples of drugs that inhibit topoisom-erase II (c). The consequence is inhibited ability of affected cells to repair DNA strand breaks. This stops the cell cycle in G2. The taxoids (eg, paclitaxel) impair mitosis (b), but by stabilizing assembled microtubules rather than by exerting a vinca alkaloid-like inhibitionof microtubular assembly

Question 11

The oncology team has treated many patients with acute lymphocytic leukemia using a combination of One drug tends to cause a high incidence of lumbar and abdominal pain, s ignificant increases of plasma amylase and transaminase activity, and other symptoms of hepatic and/or pancreatic dysfunction. Some patients developed serious hypersensitivity reactions upon drug administration, and there have been occasional sudden deaths. Which drug best fi ts this description?

A	Asparaginase
B	Azathioprine
C	Doxorubicin
D	Methotrexate
E	Vincristine

Question 11 Explanation:

Asparaginase is an enzyme that catalyzes the hydrolysis of plasma asparagine to aspartic acid and ammonia. Major toxicities from asparaginase are related to antigenicity (it is a foreign protein, and some fatal anaphylactic reactions have occurred), pancreatitis, and a 50% incidence of some hepatic dysfunction based on the presence of elevated transaminases. The drug, which is largely G1 phase-specific, is not cytotoxic to cells other than leukemic lymphoblasts. Host (and other cells) can synthesize and replace asparagine that has been hydrolyzed by the drug; the lymphoblasts cannot, and so they are killed. The responses cited are not typical of azathioprine (b), doxorubicin (c) or other antibiotic anticancer agents, methotrexate (d), or the vinca alkaloids (eg, vincristine, e).

Question 12

A 30-year-old woman being treated for ovarian cancer develops high frequency hearing loss and declining renal function in response to anticancer drug Which drug i s the most l ikely cause?

A	Bleomycin
B	Cisplatin
C	Doxorubicin
D	5-Fluorouracil
E	Paclitaxel

Question 12 Explanation:

Cisplatin, which is sometimes classified along with traditional alkylating agents, is unique among all the common anticancer agents in terms of the relative incidence of hearing loss (ototoxicity) and nephrotoxicity. You are correct in associating vincristine with hearing loss, but nephrotoxicity is very rare; in contrast, you may have recalled that methotrexate can cause nephrotoxicity, but it does not cause hearing loss, and it is indicated for a variety of cancers, but not ovarian. Bleomycin’s (a) main targeted toxicity is the lungs (pulmonary infiltrates, fibrosis, etc). Doxorubicin (c), as noted elsewhere, is cardiotoxic. The drug is mainly used for testicular carcinomas, squamous cell cancers, and lymphomas. 5-FU (d), a pyrimidine antimetabolite, is used for a variety of solid tumors. However, peripheral neuritis or neuropathy (and, especially, hearing loss) or renal damage are uncommon; rather, there is a relatively high incidence of bone marrow suppression and oral and GI mucosal damage. Paclitaxel (e) is a microtubular stabilizing drug (and plant alkaloid). It is considered first-line for some patients with advanced ovarian cancer or non-small-cell lung cancers, causes dose-dependent bone marrow suppression and peripheral neuropathy, and a fairly high incidence of acute infusion-related hypersensitivity reactions (probably due to the vehicle in which the drug is delivered).

Question 13

A 41-year-old woman comes to the outpatient area of the hematology-oncology center for her fi rst course of adjuvant chemotherapy for metastatic breast cancer following a left modified radical mastectomy and axillary lymph node dissection for infiltrating ductal carcinoma of the Two biopsies were positive for cancer. Following premedication with dexamethasone and ondansetron, she will receive combination chemotherapy with doxorubicin, cyclophosphamide, and fluorouracil. Twenty-four hours after the fi rst course of chemotherapy she will start a 10-day regimen with fi lgrastim. What i s the most l ikely reason for administering the fi lgrastim?

A	Control of nausea and emesis
B	Potentiate the anticancer effects of the chemotherapeutic agents
C	Prevent doxorubicin-induced cardiotoxicity
D	Reduce the ri sk/severity of chemo-induced neutropenia, and related infections
E	Stimulate the gastric mucosa to repair damage caused by the chemotherapy drugs

Question 13 Explanation:

Filgrastim, also known as granulocyte colony-stimulating factor (GCSF), enhances neutrophil production. One use, therefore, is to prevent neutropenia and infection associated with bone marrow depression from cancer chemotherapy. (Hint: Look at the generic name, filgrastim: granu-locyte stimulating.) The drug lacks antiemetic effects (a), potentiates the chemotherapeutic actions of no drug (b), and has no effect on doxorubicin-mediated cardiotoxicity (c) or on chemotherapy-related adverse effects on the gastric mucosa (e).

Question 14

A cancer patient receives prophylactic allopurinol before a course of chemotherapy. What i s the main reason for giving the allopurinol?

A	Facilitate host cell detoxification of the chemotherapeutic drug, thereby reducing host cell toxicities
B	Inhibit the potential for DNA repair, by topoisomerases, that otherwise might lead to chemotherapy failure
C	Potentiate the action of a nitrogen mustard or nitrosourea to bind to (cross-link) purine moieties in DNA strands
D	Prevent myelosuppression and related blood dyscrasias
E	Reduce the ri sk of hyperuricemia and i ts main consequences (renal damage, gout) that can occur with a massive cell ki l l

Question 14 Explanation:

Hyperuricemia is associated with many cancers and is a common outcome of massive cell kills induced by chemotherapeutic drugs, especially with blood-involved (disseminated) cancers such as leukemias. The uric acid is derived from cellular purine degradation, eventually formed from hypoxanthine and xanthine via xanthine oxidase, the enzyme that is inhibited by allopurinol. Recall that renal damage (and other damage, such as gout) is due to uric acid’s poor solubility in body fluids, especially at low pH. Allopurinol has no effect on the P450 system or on cellular transitions from one phase of the cell cycle to another. There is no effect on DNA synthesis or repair, or any direct cytoprotective effect on myeloid or other tissues. Be sure to remember that the metabolic detoxification of azathioprine and its active metabolite 6-mercaptopurine (itself an anticancer drug) depends in part on xanthine oxidase. Inhibiting that enzyme with allopurinol (or the relatively new related xanthine oxidase inhibitor, febuxostat), therefore, may increase the risk of toxicity to host cells.

Question 15

The FDA requires manufacturers of an anticancer drug to avoid concomitant administration of certain SSRI antidepressants (fluoxetine, paroxetine, and sertraline) to woman receiving a particular anticancer The drug in question i s mainly used to treat certain types of breast cancers and i s also used to prevent breast cancer recurrence. It commonly causes hot flashes and i s associated with a high incidence of nausea and vomiting. The SSRIs l i sted above are strong inhibitors of CYP2D6 and so they can interfere with the anticancer drug’s metabolic activation, which i s required for their chemotherapeutic effects. Which drug i s the most l ikely target of interactions with these SSRIs?

A	Bleomycin
B	Interferon alpha
C	Mercaptopurine
D	Tamoxifen.
E	Vinblastine

Question 15 Explanation:

Of all the drugs listed as possible answers, only tamoxifen, a selective estrogen receptor modifier (SERM), fits the description: it requires metabolic activation for anticancer effects (the active metabolite is about 100-times more potent than tamoxifen itself), it is indicated for estrogen-sensitive breast carcinoma (treatment or prophylaxis against recurrence), is associated with a high incidence of severe nausea and vomiting, and tends to cause hot flashes in many women (typically a delayed response occurring late in, or after, treatment with tamoxifen). Data suggest that women taking one of the listed SSRIs with tamoxifen, used for breast cancer prophylaxis, have higher rates of recurrence than those taking other SSRIs, or no antidepressants at all. The interaction does not apply to bleomycin (a), interferons (b), mercaptopurine (c; although mercaptopurine is a critical target of certain drug interactions, discussed elsewhere), or vinca alkaloids (eg, vinblastine, e). Note: It should not be surprising that many women who have cancer, or are at risk of recurrences, might benefit from an antidepressant, and SSRIs generally are the preferred drugs. Fluoxetine, paroxetine, and sertra-line interact adversely with tamoxifen, due to strong CYP2D6 inhibition, not all SSRIs do. Citalopram, escitalopram, and fluvoxamine are not strong 2D6 inhibitors, and so they are generally preferred when concomitant SSRI therapy is warranted.

Question 16

Allopurinol or the newer related drug febuxostat i s commonly administered before initiating chemotherapy of leukemias and other blood- based cancers to prevent hyperuricemia and i ts It i s also important in preventing hyperuricemia in response to chemotherapy of some solid tumors. However, i t may potentiate the host toxicity of certain anticancer drugs by inhibiting their metabolic inactivation and detoxification. With which drug should concomitant use of allopurinol or febuxostat be avoided?

A	Bleomycin
B	Cisplatin
C	Cyclophosphamide
D	Doxorubicin
E	Mercaptopurine

Question 16 Explanation:

Mercaptopurine is a (thio)purine antimetabolite that is metabolically inactivated (detoxified) by xanthine oxidase. This purine degradation pathway in which xanthine oxidase participates not only leads to formation of uric acid, but also is important to reducing host cell toxicity to the thiopurines. Thus, concomitant use of allopurinol increases the risk of host cell toxicity. The same applies to the newest approved xanthine oxidase inhibitor, febuxostat. Note that azathioprine (an inhibitor of B and T lymphocyte proliferation, typically used as an immunosuppressant) is metabolized to mercaptopurine. As a result, its metabolism is also inhibited by allopurinol. The metabolism of the other drugs listed is not xanthine oxidase-dependent, and so is not affected by allopurinol.

Question 17

A 48-year-old patient was in renal failure, but fortunately she received a kidney We start her on cyclosporine to reduce the ri sk of graft rejection. What are the most common and worrisome adverse responses associated with this immunosuppressant?

A	Cardiotoxicity and hepatotoxicity
B	Hepatotoxicity and nephrotoxicity
C	Hypotension and pulmonary fibrosis
D	Nephrotoxicity and infection ri sk
E	Thrombosis and pulmonary embolism or i schemic stroke

Question 17 Explanation:

Nephrotoxicity, or at least some clinically significant degree of renal dysfunction, occurs in about 8 of 10 patients receiving cyclosporine. It is typically dose-dependent and, particularly in renal transplant patients, could be due to either the drug (too much) or to rejection. Infection occurs about as often as renal dysfunction. Cyclosporine can cause hepatotoxicity (a), but the incidence is far lower than that of adverse renal responses or infection. Cardiotoxicity is not an issue. Blood pressure changes (c) can occur, but with cyclosporine the change more likely involves increased pressure. Cardiac or pulmonary toxicities and thromboembolism (e) due to the drug itself are extremely uncommon.

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II. Preview all questions below

1.While reviewing charts in a general medicine cl inic you see that a patient, 55-year-old and with no history of cancer at all, i s taking methotrexate (MTX). What i s the most l ikely condition for which this “anticancer drug” i s being given?

Asthma or emphysema
Hyperthyroidism
Hyperuricemia or cl inical gout
Myasthenia gravis
Rheumatoid arthritis or psoriasis

2. A 47-year-old woman with choriocarcinoma i s treated with methotrexate (MTX), given at dosages that you believe may cause s ignificant host cell Which drug would you give to l imit the toxic effects of the drug on normal host cells?

Deferoxamine
Leucovorin
N-acetylcysteine
Penicillamine
Vitamin K

3. You order vincristine, the prototype of the vinca alkaloids, to a patient with a tumor that i s l ikely to be responsive to this What i s the most l ikely adverse response to this drug?

Nephrotoxicity, renal dysfunction or failure
Neutropenia
Peripheral sensory and motor neuropathy
Pulmonary damage
Thrombocytopenia, bleeding

4. A cancer patient develops severe, i rreversible cardiomyopathy because the maximum l i fetime dose of an anticancer drug was exceeded. What drug was most l ikely responsible for this?

Asparaginase
Bleomycin
Cisplatin
Cyclophosphamide Doxorubicin
Vincristine

5. A patient with Wilms tumor i s receiving a chemotherapeutic agent that i s described as working by intercalating into DNA strands, and that i s efficacious regardless of which stage of the cell cycle the tumor cells are Which drug best fi ts this description?

Anastrozole
Cytarabine (cytosine arabinoside)
Doxorubicin
Fluorouracil.
Tamoxifen

6. A 42-year-old woman i s diagnosed with metastatic breast You consider use of tamoxifen, toremifene, or fulvestrant. Why might fulvestrant be the best choice, all other factors being equal?

Exerts antiplatelet, rather than thrombotic, effects
Lacks ability to cause hot flashes or other disturbing s ide effects
Lower ri sk of causing endometrial cancer
Provides cl inical cure, rather than palliation, in all patients
Significantly improves mineral density in, strength of, long bones

7. A patient with chronic myelogenous leukemia (CML) i s being treated with Which s ide effect or other s i tuation should you anticipate in response to imatinib therapy?

A high rate of therapeutic failure, and the need to switch to interferons α-2a and -2b
Hypotension and hypovolemia due to s ignificant drug-induced diuresis
Interactions with other drugs that depend on or affect the cytochrome P450 system
Significant toxicity to normal host cells due to profound inhibition of tyrosine kinase
Thrombocytosis, with a high ri sk of intravascular clotting

8. As a rule, large (and older) solid tumors are more difficult to eradicate when chemotherapy i s Which tumor-based property explains best the reason for this chemotherapeutic l imitation?

Growth fraction s lows, more cells enter G₀
Higher tumor blood flow washes away anticancer drugs faster
P-glycoprotein activity decreases as tumors get older
Their higher metabolic rate makes them less vulnerable to chemotherapeutic agents
Topoisomerase activity (ability to self-repair DNA strand damage) increases with tumor s i ze

9. A man has prostate cancer that will be treated with Which drug are you most l ikely to use adjunctively when starting chemotherapy?

An aromatase inhibitor (eg, anastrozole)
Flutamide
Prednisone or another potent glucocorticoid
Tamoxifen
Testosterone

10. As part of the treatment plan for a Hodgkin disease patient we have given Which phrase best describes the anticancer mechanism of action of this drug?

Alkylates DNA, causing cross-links between parallel DNA strands
Blocks microtubular assembly and mitosis during M-phase
Inhibits topoisomerase, preventing repair of DNA strand breaks
Intercalates in DNA strands, thereby preventing DNA replication by mRNA.
Stabilizes microtubular arrays, thereby preventing mitosis

11. The oncology team has treated many patients with acute lymphocytic leukemia using a combination of One drug tends to cause a high incidence of lumbar and abdominal pain, s ignificant increases of plasma amylase and transaminase activity, and other symptoms of hepatic and/or pancreatic dysfunction. Some patients developed serious hypersensitivity reactions upon drug administration, and there have been occasional sudden deaths. Which drug best fi ts this description?

Asparaginase
Azathioprine
Doxorubicin
Methotrexate
Vincristine

12. A 30-year-old woman being treated for ovarian cancer develops high frequency hearing loss and declining renal function in response to anticancer drug Which drug i s the most l ikely cause?

Bleomycin
Cisplatin
Doxorubicin
5-Fluorouracil
Paclitaxel

13. A 41-year-old woman comes to the outpatient area of the hematology-oncology center for her fi rst course of adjuvant chemotherapy for metastatic breast cancer following a left modified radical mastectomy and axillary lymph node dissection for infiltrating ductal carcinoma of the Two biopsies were positive for cancer.

Following premedication with dexamethasone and ondansetron, she will receive combination chemotherapy with doxorubicin, cyclophosphamide, and fluorouracil. Twenty-four hours after the fi rst course of chemotherapy she will start a 10-day regimen with fi lgrastim. What i s the most l ikely reason for administering the fi lgrastim?

Control of nausea and emesis
Potentiate the anticancer effects of the chemotherapeutic agents
Prevent doxorubicin-induced cardiotoxicity
Reduce the ri sk/severity of chemo-induced neutropenia, and related infections
Stimulate the gastric mucosa to repair damage caused by the chemotherapy drugs

14. A cancer patient receives prophylactic allopurinol before a course of What i s the main reason for giving the allopurinol?

Facilitate host cell detoxification of the chemotherapeutic drug, thereby reducing host cell toxicities
Inhibit the potential for DNA repair, by topoisomerases, that otherwise might lead to chemotherapy failure
Potentiate the action of a nitrogen mustard or nitrosourea to bind to (cross-link) purine moieties in DNA strands
Prevent myelosuppression and related blood dyscrasias
Reduce the ri sk of hyperuricemia and i ts main consequences (renal damage, gout) that can occur with a massive cell ki l l

15. The FDA requires manufacturers of an anticancer drug to avoid concomitant administration of certain SSRI antidepressants (fluoxetine, paroxetine, and sertraline) to woman receiving a particular anticancer The drug in question i s mainly used to treat certain types of breast cancers and i s also used to prevent breast cancer recurrence. It commonly causes hot flashes and i s associated with a high incidence of nausea and vomiting. The SSRIs l i sted above are strong inhibitors of CYP2D6 and so they can interfere with the anticancer drug’s metabolic activation, which i s required for their chemotherapeutic effects. Which drug i s the most l ikely target of interactions with these SSRIs?

Bleomycin
Interferon alpha
Mercaptopurine
Tamoxifen.
Vinblastine

16. Allopurinol or the newer related drug febuxostat i s commonly administered before initiating chemotherapy of leukemias and other blood- based cancers to prevent hyperuricemia and i ts It i s also important in preventing hyperuricemia in response to chemotherapy of some solid tumors. However, i t may potentiate the host toxicity of certain anticancer drugs by inhibiting their metabolic inactivation and detoxification. With which drug should concomitant use of allopurinol or febuxostat be avoided?

Bleomycin
Cisplatin
Cyclophosphamide
Doxorubicin
Mercaptopurine

17. A 48-year-old patient was in renal failure, but fortunately she received a kidney We start her on cyclosporine to reduce the ri sk of graft rejection. What are the most common and worrisome adverse responses associated with this immunosuppressant?

Cardiotoxicity and hepatotoxicity
Hepatotoxicity and nephrotoxicity
Hypotension and pulmonary fibrosis
Nephrotoxicity and infection ri sk
Thrombosis and pulmonary embolism or i schemic stroke

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