Anticancer Drugs Practice Questions

Q: Which of the following statements is FALSE regarding vincristine?

It does not cause alopecia.. ***It does not cause alopecia.*** - This statement is **false** because vincristine, like many chemotherapeutic agents, commonly causes **alopecia** (hair loss) due to its impact on rapidly dividing cells, including hair follicle cells. - While it may be considered less myelosuppressive than some other anticancer drugs, its effect on hair follicles is well-documented. *It is an alkaloid.* - This statement is **true** because vincristine is a **vinca alkaloid**, derived from the Madagascar periwinkle plant (*Catharanthus roseus*). - Vinca alkaloids are a class of antineoplastic agents that target microtubules. *Its use is associated with neurotoxicity.* - This statement is **true** as **neurotoxicity** is a prominent and dose-limiting side effect of vincristine, manifesting as peripheral neuropathy (e.g., paresthesias, foot drop, constipation due to autonomic neuropathy). - This adverse effect arises from its mechanism of action, which involves disrupting microtubules critical for axonal transport. *It is a useful drug for induction of remission in acute lymphoblastic leukemia.* - This statement is **true**; **vincristine** is a cornerstone of combination chemotherapy regimens for **acute lymphoblastic leukemia (ALL)**, particularly during the induction phase. - Its efficacy in ALL is attributed to its ability to arrest cell division in metaphase.

Q: Which of the following statements about vinca alkaloids is true?

Inhibits mitotic spindle. ***Inhibits mitotic spindle*** - **Vinca alkaloids** (e.g., vincristine, vinblastine) exert their cytotoxic effects by binding to **tubulin**, thereby inhibiting its polymerization into microtubules. - This disruption prevents the formation of the **mitotic spindle**, arresting cells in metaphase and leading to apoptosis. *Enhances polymerization of tubulin* - This statement describes the mechanism of action of **taxanes** (e.g., paclitaxel), which stabilize microtubules and prevent their depolymerization. - Vinca alkaloids, in contrast, **inhibit** tubulin polymerization, preventing microtubule assembly. *Inhibits topoisomerase I* - Inhibition of **topoisomerase I** is the mechanism of action for drugs like **irinotecan** and **topotecan**. - These agents cause single-strand breaks in DNA, which is distinct from the microtubule disruption caused by vinca alkaloids. *Inhibits topoisomerase II* - Drugs like **etoposide** and **teniposide** work by inhibiting **topoisomerase II**, leading to double-strand DNA breaks. - This mechanism is different from the disruption of microtubule dynamics seen with vinca alkaloids.

Q: All are true regarding Sunitinib except which of the following?

It is excreted primarily in urine. ***It is excreted primarily in urine*** - **Sunitinib** is predominantly metabolized in the **liver** by CYP3A4 and primarily excreted in the **feces**, not urine. - Its major active metabolite, N-desethyl sunitinib, is also primarily eliminated via the fecal route. *It inhibits tyrosine kinase receptors* - **Sunitinib** is a **multitargeted receptor tyrosine kinase (RTK) inhibitor**. - It blocks several RTKs involved in tumor growth, angiogenesis, and metastatic progression, such as **VEGFR, PDGFR, KIT, and FLT3**. *It is used for the treatment of GIST* - **Sunitinib** is approved for the treatment of **imatinib-refractory** or **imatinib-intolerant gastrointestinal stromal tumors (GIST)**. - Its mechanism in GIST involves inhibiting KIT and PDGFR, which are often mutated and constitutively active in this cancer. *It is used for renal cell carcinoma* - **Sunitinib** is a standard first-line treatment for **advanced renal cell carcinoma (RCC)**. - Its efficacy in RCC is primarily due to its inhibition of VEGFR, which targets the high vascularity characteristic of kidney tumors.

Q: Resistance to Methotrexate develops due to?

Increased production of dihydrofolate reductase (DHFR). ***Increased production of dihydrofolate reductase (DHFR)*** - Methotrexate acts by inhibiting **dihydrofolate reductase (DHFR)**, an enzyme essential for **folate metabolism** and DNA synthesis. - An **increased production of DHFR** (through gene amplification or overexpression) by cancer cells allows them to bypass the drug's inhibitory effects, leading to resistance. - This is the **most common mechanism** of methotrexate resistance. *Rapid proliferation of cancer cells* - While **rapid cell proliferation** is a characteristic of cancer, it doesn't directly explain resistance to methotrexate. - Methotrexate targets fast-dividing cells (S-phase specific), so rapid proliferation often makes them **more susceptible**, not resistant, as long as the drug's mechanism is effective. *Thymidylate kinase deficiency* - **Thymidylate kinase** is involved in the phosphorylation of **thymidine** to produce **dTMP** (deoxythymidine monophosphate). - A deficiency in this enzyme would likely hinder DNA synthesis, potentially increasing sensitivity to DNA-targeting agents, rather than causing resistance to methotrexate. *Thymidylate synthetase deficiency* - **Thymidylate synthetase** converts dUMP to dTMP using **5,10-methylene-THF** as a cofactor. - Methotrexate **indirectly inhibits** thymidylate synthetase by depleting tetrahydrofolate cofactor pools through DHFR inhibition. - A **deficiency** of this enzyme would not cause resistance; rather, **increased thymidylate synthetase** expression can be an alternative resistance mechanism, though less common than DHFR overexpression.

Q: Which of the following antineoplastic drugs SHOULD NOT be given by rapid IV infusion?

Cisplatin. ***Cisplatin*** - **Cisplatin** is highly nephrotoxic and emetogenic; rapid IV infusion can exacerbate these adverse effects, leading to severe renal damage and intractable nausea/vomiting. - It typically requires **prolonged infusion times** (e.g., 6-8 hours) with extensive pre- and post-hydration to reduce kidney toxicity and ensure patient tolerance. *Cyclophosphamide* - While cyclophosphamide can cause **hemorrhagic cystitis**, this is managed by adequate hydration and mesna, and its infusion rate is generally not as critically prolonged as cisplatin's. - It is often administered as a **relatively quick IV infusion** over 30-60 minutes, emphasizing hydration. *Bleomycin* - **Bleomycin** is known for pulmonary toxicity and hypersensitivity reactions, but these are not primarily linked to its infusion rate. - It is commonly given via **slow IV push or short infusion**, sometimes with a test dose to assess for hypersensitivity. *Cytosine arabinoside* - **Cytosine arabinoside** can cause myelosuppression and cerebellar toxicity, but these toxicities are not typically exacerbated by a rapid infusion rate. - It is often administered via a **continuous infusion** over several days or as a rapid IV bolus.

Q: Which of the following anticancer drugs can cause flagellate dermatitis?

Bleomycin. ***Bleomycin*** - **Flagellate dermatitis** is a characteristic skin toxicity of bleomycin, presenting as linear erythematous streaks that resemble whip marks. - This dermatological reaction is thought to be related to the drug's accumulation in the skin, leading to inflammation and hyperpigmentation. *Cisplatin* - Cisplatin is notorious for causing significant **nephrotoxicity** and **ototoxicity**, which are its dose-limiting toxicities. - While it can cause some dermatological side effects, **flagellate dermatitis** is not a common or characteristic adverse effect associated with this drug. *L-asparaginase* - L-asparaginase frequently causes **hypersensitivity reactions** and **pancreatitis** due to its mechanism of depleting asparagine. - Skin toxicities associated with L-asparaginase are typically less common and do not include **flagellate dermatitis**. *Doxorubicin* - Doxorubicin is well-known for its **cardiotoxicity**, leading to dilated cardiomyopathy, and also causes **alopecia** and severe local tissue damage if extravasated. - Although it can cause various skin manifestations, **flagellate dermatitis** is not a typical dermatological toxicity of doxorubicin.

Q: Chemotherapeutic agents in the EMA-CO regimen include all except which one of the following?

Mithramycin. ***Mithramycin*** - **Mithramycin**, also known as **plicamycin**, is not a component of the EMA-CO regimen. It is an **antineoplastic antibiotic** that inhibits RNA synthesis and has been used in the past for **testicular cancer** and **hypercalcemia of malignancy**. - Its mechanism of action and common indications differ from the drugs in the EMA-CO protocol, which are typically used for **gestational trophoblastic neoplasia**. *Etoposide* - **Etoposide** is a **topoisomerase inhibitor** and a key component of the **EMA-CO regimen**. - It works by causing **DNA strand breaks**, leading to **apoptosis** of cancer cells, and is crucial for treating **high-risk gestational trophoblastic neoplasia**. *Actinomycin-D* - **Actinomycin-D**, also known as **dactinomycin**, is another essential component of the **EMA-CO regimen**. - It is an **antibiotic chemotherapy drug** that inhibits RNA synthesis by intercalating with DNA, commonly used in various cancers, including **gestational trophoblastic neoplasia**. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** included in the **EMA-CO regimen**. - It works by forming **cross-links within DNA**, preventing cell division and leading to cancer cell death, contributing significantly to the efficacy of the regimen for **gestational trophoblastic neoplasia**.

Q: All of these are G2 phase blockers except:

Paclitaxel. ***Paclitaxel*** - **Paclitaxel** is a **microtubule-stabilizing drug** that acts predominantly in the **M phase** of the cell cycle by inhibiting microtubule depolymerization, thereby blocking cell division [1]. - It is known as a **mitotic inhibitor**, specifically preventing the progression from **metaphase to anaphase** [2]. - **NOT a G2 phase blocker** - this is the correct answer. *Etoposide* - **Etoposide** is a **topoisomerase II inhibitor** that causes DNA strand breaks, predominantly acting in the **late S and G2 phases** of the cell cycle [3]. - Its primary effect is to arrest cells in the **G2 phase**, making it a classic **G2 phase blocker** [2]. *Daunorubicin* - **Daunorubicin** is an **anthracycline antibiotic** that intercalates into DNA, leading to DNA damage and inhibition of DNA and RNA synthesis. - It primarily acts in the **S phase** but the resulting DNA damage activates checkpoints leading to **G2 phase arrest**, thus functioning as a G2 blocker [3]. *Topotecan* - **Topotecan** is a **topoisomerase I inhibitor**, which prevents DNA unwinding and replication by stabilizing the topoisomerase I-DNA complex, leading to DNA strand breaks. - Its main effect is in the **S phase**, but the DNA damage induces cell cycle arrest in the **G2 phase** through checkpoint activation [3].

Q: Which of the following is not an alkylating agent?

Cladrabine. ***Cladrabine*** - **Cladrabine** is a **purine analog**, which is a type of antimetabolite, not an alkylating agent. - It works by being incorporated into DNA, leading to **DNA strand breaks** and inhibition of DNA synthesis. *Chlorambucil* - **Chlorambucil** is a nitrogen mustard derivative, which is a classic **alkylating agent**. - It forms **covalent bonds** with DNA, primarily at guanine bases, cross-linking DNA strands and inhibiting replication. *Ifosfamide* - **Ifosfamide** belongs to the **oxazaphosphorine** class of alkylating agents, similar to cyclophosphamide. - It also works by forming **DNA cross-links**, which interferes with DNA replication and transcription. *Nitrosurea* - **Nitrosureas** (e.g., carmustine, lomustine) are a class of alkylating agents that can cross the **blood-brain barrier**. - They act by **alkylating DNA** and RNA, inducing interstrand and intrastrand cross-links, and inhibiting DNA repair.

Q: Which of the following drugs is not used in prostate carcinoma?

Testosterone. ***Testosterone*** - **Testosterone** is an **androgen** that promotes the growth and progression of prostate cancer. - Administering testosterone would worsen prostate carcinoma and is therefore contraindicated [2]. *Finasteride* - **Finasteride** is a **5-alpha-reductase inhibitor** that blocks the conversion of testosterone to dihydrotestosterone (DHT), the more potent androgen responsible for prostate growth [1]. - It is used in prostate cancer management to reduce androgen-dependent tumor growth, as DHT stimulates the proliferation of prostate cancer cells. *Diethylstilbestrol* - **Diethylstilbestrol (DES)** is a **synthetic estrogen** that works by suppressing the production of testosterone from the testes through negative feedback on the hypothalamus and pituitary gland [4]. - While historically used, its use has largely been replaced by newer, more targeted therapies due to its significant side effects [4]. *Flutamide* - **Flutamide** is an **anti-androgen** that acts by competitively blocking androgen receptors in prostate cancer cells [3]. - It prevents testosterone and DHT from binding to their receptors, thereby inhibiting androgen-dependent tumor growth without affecting androgen production [3].

Question 1

Which of the following statements is FALSE regarding vincristine?

Accepted Answer

It does not cause alopecia.

Answer

Its use is associated with neurotoxicity.

Answer

It is an alkaloid.

Answer

It is a useful drug for induction of remission in acute lymphoblastic leukemia.

Question 2

Which of the following statements about vinca alkaloids is true?

Accepted Answer

Inhibits mitotic spindle

Answer

Enhances polymerization of tubulin

Answer

Inhibits topoisomerase I

Answer

Inhibits topoisomerase II

Question 3

All are true regarding Sunitinib except which of the following?

Accepted Answer

It is excreted primarily in urine

Answer

It inhibits tyrosine kinase receptors

Answer

It is used for the treatment of GIST

Answer

It is used for renal cell carcinoma

Question 4

Resistance to Methotrexate develops due to?

Accepted Answer

Increased production of dihydrofolate reductase (DHFR)

Answer

Rapid proliferation of cancer cells

Answer

Thymidylate kinase deficiency

Answer

Thymidylate synthetase deficiency

Question 5

Which of the following antineoplastic drugs SHOULD NOT be given by rapid IV infusion?

Accepted Answer

Cisplatin

Answer

Cyclophosphamide

Answer

Cytosine arabinoside

Answer

Bleomycin

Question 6

Which of the following anticancer drugs can cause flagellate dermatitis?

Accepted Answer

Bleomycin

Answer

Cisplatin

Answer

L-asparaginase

Answer

Doxorubicin

Question 7

Chemotherapeutic agents in the EMA-CO regimen include all except which one of the following?

Accepted Answer

Mithramycin

Answer

Etoposide

Answer

Actinomycin-D

Answer

Cyclophosphamide

Question 8

All of these are G2 phase blockers except:

Accepted Answer

Paclitaxel

Answer

Daunorubicin

Answer

Etoposide

Answer

Topotecan

Question 9

Which of the following is not an alkylating agent?

Accepted Answer

Cladrabine

Answer

Chlorambucil

Answer

Ifosfamide

Answer

Nitrosurea

Question 10

Which of the following drugs is not used in prostate carcinoma?

Accepted Answer

Testosterone

Answer

Diethylstilbestrol

Answer

Flutamide

Answer

Finasteride

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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