Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 501: Which of the following anti-cancer drugs is NOT S-phase specific?

A. Methotrexate
B. Mercaptopurine
C. Ifosfamide (Correct Answer)
D. Thioguanine

Explanation: **Explanation:** The cell cycle specificity of anticancer drugs is a high-yield concept for NEET-PG. Anticancer agents are broadly classified into **Cell Cycle-Specific (CCS)** and **Cell Cycle-Non-Specific (CCNS)** drugs. **Why Ifosfamide is the correct answer:** Ifosfamide is an **alkylating agent** (a nitrogen mustard derivative). Alkylating agents work by covalently bonding alkyl groups to DNA bases (primarily Guanine), leading to DNA cross-linking and strand breaks. This mechanism occurs regardless of whether the cell is actively dividing or resting. Therefore, Ifosfamide is **Cell Cycle-Non-Specific (CCNS)**. While it is most toxic to cells in the late G1 or S phase, it does not target a specific phase to exert its action. **Why the other options are incorrect:** * **Methotrexate:** An antimetabolite that inhibits *Dihydrofolate Reductase (DHFR)*. It prevents the synthesis of tetrahydrofolate, which is essential for thymidylate and purine synthesis. This process is strictly required during DNA synthesis, making it **S-phase specific**. * **Mercaptopurine (6-MP) & Thioguanine (6-TG):** These are purine analogues. They act as "fraudulent nucleotides" that incorporate into DNA/RNA or inhibit *de novo* purine synthesis. Since DNA replication occurs during the **S-phase**, these drugs are phase-specific. **High-Yield Clinical Pearls for NEET-PG:** 1. **Acrolein Toxicity:** Both Ifosfamide and Cyclophosphamide produce a toxic metabolite called **Acrolein**, which causes **Hemorrhagic Cystitis**. 2. **Prevention:** Hemorrhagic cystitis is prevented by aggressive hydration and **MESNA** (2-Mercaptoethane sulfonate Na), which neutralizes acrolein in the bladder. 3. **Mnemonic for S-phase drugs:** "It’s **S**mart to **MET** at the **PUR**ine **PYR**amid" (**MET**hotrexate, **PUR**ines like 6-MP/6-TG, **PYR**imidines like 5-FU/Cytarabine).

Question 502: All of the following side effects are produced by Cisplatin except?

A. Ototoxicity
B. Nephrotoxicity
C. Coasting effect
D. Pulmonary fibrosis (Correct Answer)

Explanation: **Explanation:** **Cisplatin** is a potent platinum-based alkylating agent used for various solid tumors. The correct answer is **Pulmonary fibrosis**, as this is a classic dose-limiting toxicity associated with **Bleomycin** and **Busulfan**, not Cisplatin. **Why the other options are incorrect (Side effects of Cisplatin):** * **Nephrotoxicity:** This is the most significant dose-limiting toxicity of Cisplatin. It causes acute tubular necrosis. It is managed with aggressive **amifostine** (a cytoprotective agent) and pre-treatment hydration. * **Ototoxicity:** Cisplatin causes high-frequency hearing loss and tinnitus due to damage to the hair cells in the cochlea. This is often irreversible. * **Coasting Effect:** This refers to a unique phenomenon seen with Cisplatin-induced peripheral neuropathy where the neurological symptoms continue to worsen for several weeks even after the drug has been discontinued. * **Emetogenicity:** Though not listed as an option, Cisplatin is the most highly emetogenic chemotherapy drug, requiring prophylaxis with 5-HT3 antagonists (e.g., Ondansetron) and Aprepitant. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Cisplatin toxicity:** "PON" – **P**eripheral neuropathy, **O**totoxicity, **N**ephrotoxicity. * **Carboplatin** is a related drug that is less nephrotoxic and ototoxic but causes more significant **myelosuppression** (thrombocytopenia). * **Oxaliplatin** is notorious for causing **cold-induced peripheral neuropathy**. * To prevent Cisplatin-induced nephrotoxicity, always remember: **Hydration + Chloride diuresis + Amifostine.**

Question 503: Mucositis is a common side effect of which of the following chemotherapeutic agents?

A. 5-Fluorouracil (Correct Answer)
B. Methotrexate
C. Paclitaxel
D. Cisplatin

Explanation: **Explanation:** **Mucositis** refers to the inflammatory and ulcerative inflammation of the mucous membranes lining the digestive tract. It is a hallmark toxicity of drugs that interfere with the synthesis of pyrimidines and DNA, particularly those with a high affinity for rapidly dividing gastrointestinal epithelium. **1. Why 5-Fluorouracil (5-FU) is the Correct Answer:** 5-FU is an antimetabolite (pyrimidine analog) that inhibits **thymidylate synthase**, leading to "thymineless death" of cells. It is notorious for causing severe **gastrointestinal toxicity**, specifically oral and intestinal mucositis and diarrhea. This occurs because the drug prevents the rapid turnover of the mucosal lining. In clinical practice, ice chips (oral cryotherapy) are often used during 5-FU bolus administration to reduce the risk of mucositis. **2. Analysis of Incorrect Options:** * **Methotrexate:** While Methotrexate can cause mucositis, it is more classically associated with **bone marrow suppression** and nephrotoxicity. In the context of standard NEET-PG questions, 5-FU is the "textbook" prototype for severe mucositis. * **Paclitaxel:** A taxane that inhibits microtubule disassembly. Its dose-limiting toxicity is **peripheral neuropathy** and neutropenia. * **Cisplatin:** A platinum compound primarily known for its **nephrotoxicity**, ototoxicity, and being highly **emetogenic** (vomiting), rather than causing primary mucositis. **Clinical Pearls for NEET-PG:** * **5-FU + Leucovorin:** Leucovorin *enhances* the activity of 5-FU (unlike its role in "rescuing" cells from Methotrexate). * **Hand-Foot Syndrome:** Another high-yield side effect of 5-FU (and its prodrug Capecitabine). * **DPD Deficiency:** Patients deficient in Dihydropyrimidine dehydrogenase (DPD) experience life-threatening toxicity when given 5-FU.

Question 504: What is the key difference between Cisplatin and Carboplatin?

A. Cisplatin has more nephrotoxic side effects compared to Carboplatin (Correct Answer)
B. Cisplatin is less neurotoxic than Carboplatin
C. Carboplatin is more neurotoxic than Cisplatin
D. Cisplatin causes fewer gastric issues compared to Carboplatin

Explanation: ***Cisplatin has more nephrotoxic side effects compared to Carboplatin*** - This is the **KEY clinical difference** between these platinum-based chemotherapy agents - Cisplatin causes **severe nephrotoxicity** requiring aggressive hydration and electrolyte monitoring - Carboplatin has **minimal renal toxicity**, making it safer in patients with renal impairment - This difference is why Carboplatin is often preferred when nephrotoxicity is a concern *Cisplatin is less neurotoxic than Carboplatin* - This is INCORRECT - the reverse is true - Cisplatin causes MORE neurotoxicity (peripheral neuropathy, ototoxicity) - Carboplatin has significantly less neurotoxicity *Carboplatin is more neurotoxic than Cisplatin* - This is INCORRECT - Carboplatin is actually LESS neurotoxic than Cisplatin - Neurotoxicity (including ototoxicity) is a major dose-limiting toxicity of Cisplatin, not Carboplatin *Cisplatin causes fewer gastric issues compared to Carboplatin* - This is INCORRECT - Cisplatin is one of the MOST emetogenic chemotherapy agents - Carboplatin causes significantly less nausea and vomiting than Cisplatin - The primary toxicity of Carboplatin is **myelosuppression (thrombocytopenia)**, not GI effects **Summary of Key Differences:** - **Cisplatin:** More nephrotoxic, more neurotoxic, more emetogenic - **Carboplatin:** Less nephrotoxic, less neurotoxic, less emetogenic, MORE myelosuppressive

Question 505: Which adverse effect of Bleomycin is exacerbated by radiation exposure?

A. Neural toxicity
B. Hepatotoxicity
C. Gastric toxicity
D. Pulmonary toxicity (Correct Answer)

Explanation: ***Pulmonary toxicity*** - Bleomycin is well-known for causing dose-dependent **pulmonary fibrosis**. It damages **type I pneumocytes**, leading to inflammation, proliferation of **type II pneumocytes**, and eventual fibrosis, impairing gas exchange. - The risk of pulmonary toxicity is significantly increased by concurrent or prior **chest radiation therapy** and administration of high concentrations of supplemental **oxygen**, as both are also injurious to lung tissue. *Gastric toxicity* - Bleomycin is not typically associated with significant gastric toxicity. Common side effects are milder and include **mucositis** and **stomatitis** rather than severe gastric damage. - There is no evidence of a synergistic toxic effect on the gastric mucosa when Bleomycin is combined with radiation therapy. *Neural toxicity* - Neurotoxicity is not a characteristic side effect of Bleomycin. Chemotherapeutic agents like **vincristine** and **cisplatin** are more commonly associated with peripheral neuropathy. - While radiation can cause nerve damage, this is not a known interaction that is specifically exacerbated by Bleomycin administration. *Hepatotoxicity* - Severe liver damage (**hepatotoxicity**) is a rare side effect of Bleomycin. Mild and transient elevations of liver enzymes may occur but are not clinically significant. - Unlike the lungs, the liver is not a primary site for synergistic toxicity between Bleomycin and radiation therapy.

Question 506: What is the primary mechanism of action of methotrexate?

A. Inhibits RNA synthesis by blocking RNA polymerase
B. Inhibits dihydrofolate reductase, leading to decreased DNA synthesis (Correct Answer)
C. Interferes with microtubule formation during cell division
D. Inhibits DNA synthesis by blocking thymidylate synthase

Explanation: ***Inhibits dihydrofolate reductase, leading to decreased DNA synthesis***- **Methotrexate (MTX)** is a **folate analog** that acts as a potent competitive inhibitor of the enzyme **dihydrofolate reductase (DHFR)**.- Inhibition of **DHFR** prevents the conversion of **dihydrofolate** to **tetrahydrofolate (THF)**, which is crucial for the synthesis of **purines** and **thymidylate**, halting DNA and RNA production.*Inhibits DNA synthesis by blocking thymidylate synthase*- This mechanism of action is primarily associated with the fluorinated pyrimidine analog **5-Fluorouracil (5-FU)**.- **5-FU** acts as a suicide substrate that irreversibly inhibits **thymidylate synthase**, not dihydrofolate reductase.*Inhibits RNA synthesis by blocking RNA polymerase*- While MTX affects nucleotide synthesis (building blocks for RNA), its primary and most impactful target is **DHFR**, affecting DNA synthesis prominently.- Direct blocking of **RNA polymerase** is the mechanism for drugs such as **Actinomycin D** (by DNA intercalation).*Interferes with microtubule formation during cell division*- This mechanism belongs to the class of **microtubule-targeting agents**, such as **vinca alkaloids** (**vincristine**) and **taxanes** (**paclitaxel**).- These agents disrupt the formation or disassembly of the **mitotic spindle**, leading to **mitotic arrest**, which is distinct from the mechanism of methotrexate.

Question 507: Which of the following drugs are used to treat chemotherapy-induced nausea and vomiting?

A. Doxylamine + domperidone + aprepitant
B. Prochlorperazine + metoclopramide + domperidone
C. Dexamethasone + metoclopramide + domperidone
D. Granisetron + dexamethasone + aprepitant (Correct Answer)

Explanation: ***Granisetron + dexamethasone + aprepitant***- This triple-therapy combination represents the gold standard for preventing and treating highly emetogenic chemotherapy (HEC)-induced nausea and vomiting (CINV).- **Granisetron** (a **5-HT3 receptor antagonist**) blocks acute CINV, **dexamethasone** (a corticosteroid) enhances the antiemetic effect, and **aprepitant** (an **NK-1 receptor antagonist**) covers the delayed phase of CINV.*Doxylamine + domperidone + aprepitant*- **Doxylamine** is primarily used for nausea in pregnancy (mixed with pyridoxine) and is not a standard first-line agent for CINV prophylaxis.- **Domperidone** (a D2 antagonist) is infrequently used for CINV due to concerns over QT prolongation and is significantly less effective than 5-HT3 antagonists.*Prochlorperazine + metoclopramide + domperidone*- This combination consists primarily of **dopamine D2 receptor antagonists** and is insufficient for prophylaxis against moderately or highly emetogenic chemotherapy.- It lacks both a **5-HT3 inhibitor** (crucial for acute CINV) and an **NK-1 inhibitor** (crucial for delayed CINV and highly emetogenic regimens).*Dexamethasone + metoclopramide + domperidone*- This regimen is missing the key highly potent antiemetics: the **5-HT3 receptor antagonist** (like granisetron or ondansetron) and the **NK-1 receptor antagonist** (like aprepitant), which are indispensable for highly emetogenic chemotherapy.- While **dexamethasone** is standard, relying solely on **metoclopramide** and **domperidone** (D2 antagonists) is an inadequate primary strategy against severe CINV.

Question 508: A patient with tumor lysis syndrome has elevated uric acid levels. What is the mechanism of action of pegloticase?

A. Urat-1 receptor inhibition
B. Oxidises uric acid (Correct Answer)
C. Xanthine oxidase inhibition
D. Excretion of uric acid

Explanation: ***Oxidises uric acid*** - Pegloticase is a recombinant pegylated uricase enzyme that directly catalyzes the conversion of highly insoluble **uric acid**. - It oxidizes uric acid into **allantoin**, which is a highly soluble compound easily excreted by the kidneys, effectively lowering serum uric acid levels. *Xanthine oxidase inhibition* - This is the mechanism of action for drugs like **allopurinol** and **febuxostat**, used to prevent the formation of uric acid. - These agents act upstream by inhibiting the enzyme responsible for synthesizing uric acid from xanthine and hypoxanthine. *URAT1 receptor inhibition* - URAT1 inhibitors (**lesinurad**) prevent the reabsorption of native uric acid from the renal tubules back into the bloodstream. - This mechanism is characteristic of **uricosuric agents**, which increase the renal clearance of uric acid. *Excretion of uric acid* - While pegloticase ultimately facilitates excretion (as allantoin), this option is too broad; its primary action is **enzymatic conversion**. - Direct excretion of native uric acid is increased by **uricosuric drugs** (e.g., probenecid), not by pegloticase's oxidative action.

Question 509: Which of the following statements regarding Thalidomide is correct? a. It acts as an antimetabolite and is useful as an immunosuppressant b. It is used in the treatment of multiple myeloma c. It is used in the management of Type 2 lepra reaction (ENL) d. It is teratogenic

A. a, b, d
B. a, b, c
C. a, c, d
D. b, c, d (Correct Answer)

Explanation: ***b, c, d*** - Statements b, c, and d are correct: Thalidomide is an **Immunomodulatory Drug (IMiD)** used effectively in the treatment of **multiple myeloma**, it is the drug of choice for **Erythema Nodosum Leprosum (ENL)** (Type 2 lepra reaction), and it is historically significant for causing **phocomelia** (teratogenicity). - Its mechanism involves downregulation of **pro-inflammatory cytokines** like TNF-alpha, which underlies its use in ENL, and anti-angiogenic/anti-proliferative effects against myeloma cells. *a, b, c* - Statement 'a' is incorrect because Thalidomide is an **Immunomodulatory Drug (IMiD)**, not an **antimetabolite** (a class of drugs that inhibit DNA/RNA synthesis). - Inclusion of the incorrect mechanism ('a') invalidates this set, despite 'b' (multiple myeloma) and 'c' (ENL) being correct clinical applications. *a, c, d* - This combination is incorrect primarily because it includes statement 'a', which wrongly defines Thalidomide as an **antimetabolite**. - Crucially, this option omits statement 'b', which is a major, current indication for Thalidomide in **multiple myeloma**. *a, b, d* - This combination wrongly includes the factual error of statement 'a' (it is not an **antimetabolite**). - It also misses statement 'c', which is the prominent use of Thalidomide in **Type 2 lepra reaction (ENL)**.

Question 510: Which one of the following drugs is most effective in the treatment of gestational trophoblastic neoplasia?

A. Actinomycin D
B. Cisplatin
C. Gemcitabine
D. Methotrexate (Correct Answer)

Explanation: ***Methotrexate*** - **Methotrexate** is the most commonly used first-line chemotherapy for **low-risk gestational trophoblastic neoplasia (GTN)**, with cure rates exceeding 90% as a single agent. - It works by inhibiting **dihydrofolate reductase**, thereby blocking DNA synthesis and cell proliferation in rapidly dividing trophoblastic cells. - Administered as a single agent in various regimens (weekly IM, 5-day course, or 8-day alternating with folinic acid). *Actinomycin D* - **Actinomycin D** is an equally effective alternative first-line agent for low-risk GTN with similar cure rates to methotrexate. - However, the question asks for the "most effective," and both drugs have comparable efficacy; methotrexate is often preferred initially due to its favorable side effect profile and ease of administration. - Actinomycin D is frequently used when methotrexate resistance develops or as part of combination therapy for high-risk disease. *Cisplatin* - **Cisplatin** is a platinum-based chemotherapy drug reserved for **high-risk or resistant GTN**, typically as part of multi-drug regimens like EMA-CO (Etoposide, Methotrexate, Actinomycin D, Cyclophosphamide, Vincristine). - While effective in combination therapy, it is not used as first-line monotherapy for GTN. *Gemcitabine* - **Gemcitabine** is an antimetabolite used in various cancers but is **not a standard drug** for GTN treatment. - It may be considered for **refractory or resistant cases** as part of salvage therapy, but is not part of standard first-line or second-line protocols for GTN.

Practice by Chapter

Principles of Cancer Chemotherapy

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Alkylating Agents

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Antimetabolites

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Antitumor Antibiotics

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Plant Alkaloids

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Topoisomerase Inhibitors

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Hormonal Agents

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Targeted Therapy

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Immunotherapy

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Management of Chemotherapy Side Effects

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