Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 571: Which of the following statements about vinca alkaloids is true?

A. Inhibits mitotic spindle (Correct Answer)
B. Enhances polymerization of tubulin
C. Inhibits topoisomerase I
D. Inhibits topoisomerase II

Explanation: ***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.

Question 572: All are true regarding Sunitinib except which of the following?

A. It inhibits tyrosine kinase receptors
B. It is excreted primarily in urine (Correct Answer)
C. It is used for the treatment of GIST
D. It is used for renal cell carcinoma

Explanation: ***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.

Question 573: Which of the following antineoplastic drugs SHOULD NOT be given by rapid IV infusion?

A. Cyclophosphamide
B. Cytosine arabinoside
C. Cisplatin (Correct Answer)
D. Bleomycin

Explanation: ***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.

Question 574: Resistance to Methotrexate develops due to?

A. Rapid proliferation of cancer cells
B. Thymidylate kinase deficiency
C. Thymidylate synthetase deficiency
D. Increased production of dihydrofolate reductase (DHFR) (Correct Answer)

Explanation: ***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.

Question 575: Which of the following anticancer drugs can cause flagellate dermatitis?

A. Cisplatin
B. Bleomycin (Correct Answer)
C. L-asparaginase
D. Doxorubicin

Explanation: ***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.

Question 576: All of these are G2 phase blockers except:

A. Paclitaxel (Correct Answer)
B. Daunorubicin
C. Etoposide
D. Topotecan

Explanation: ***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].

Question 577: Chemotherapeutic agents in the EMA-CO regimen include all except which one of the following?

A. Etoposide
B. Mithramycin (Correct Answer)
C. Actinomycin-D
D. Cyclophosphamide

Explanation: ***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**.

Question 578: Which of the following is not an alkylating agent?

A. Chlorambucil
B. Ifosfamide
C. Nitrosurea
D. Cladrabine (Correct Answer)

Explanation: ***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.

Question 579: Which of the following drugs is not used in prostate carcinoma?

A. Diethylstilbestrol
B. Flutamide
C. Testosterone (Correct Answer)
D. Finasteride

Explanation: ***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 580: Which of the following is used to treat hormone-responsive breast cancer?

A. Clomiphene citrate
B. Diethylstibestrol
C. Tamoxifen (Correct Answer)
D. Cyproterone acetate

Explanation: ***Tamoxifen*** - **Tamoxifen** is a **selective estrogen receptor modulator (SERM)** that acts as an **estrogen antagonist** in breast tissue, thereby blocking estrogen's proliferative effects on breast cancer cells. - It is a cornerstone treatment for **hormone-responsive (estrogen receptor-positive, ER+) breast cancer**, both in early and advanced stages, and can also be used for prevention in high-risk individuals. *Cyproterone acetate* - **Cyproterone acetate** is an **anti-androgen** with progestational activity, primarily used in conditions like **hirsutism**, prostate cancer, and severe acne. - While it has hormonal activity, it is not a primary therapeutic agent for **hormone-responsive breast cancer**. *Clomiphene citrate* - **Clomiphene citrate** is an **estrogen receptor modulator** used to induce ovulation in women who are anovulatory or oligo-ovulatory. - It works by blocking estrogen receptors in the hypothalamus, leading to increased release of **gonadotropins**, and is not used in breast cancer treatment. *Diethylstibestrol* - **Diethylstilbestrol (DES)** is a **synthetic non-steroidal estrogen** that was historically used for various conditions, including preventing miscarriage, but was later found to have significant adverse effects and teratogenic risks. - It was used as a treatment for advanced prostate cancer and, in very specific circumstances, even for breast cancer in postmenopausal women, but it is **not a current first-line therapy** for hormone-responsive breast cancer due to its toxicity and the availability of safer, more effective drugs.

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

Practice Questions

Antimetabolites

Practice Questions

Antitumor Antibiotics

Practice Questions

Plant Alkaloids

Practice Questions

Topoisomerase Inhibitors

Practice Questions

Hormonal Agents

Practice Questions

Targeted Therapy

Practice Questions

Immunotherapy

Practice Questions

Management of Chemotherapy Side Effects

Practice Questions

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