Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 391: Cetuximab, an EGFR antagonist, can be used in which of the following conditions?

A. Palliation in head and neck cancer (Correct Answer)
B. Anal canal carcinoma
C. Gastric carcinoma
D. Lung carcinoma

Explanation: **Explanation:** **Cetuximab** is a recombinant human/mouse chimeric monoclonal antibody that binds specifically to the extracellular domain of the **Epidermal Growth Factor Receptor (EGFR)**. By inhibiting EGFR, it blocks downstream signaling pathways (like KRAS/MAPK) that promote cell proliferation and survival. **1. Why Option A is correct:** Cetuximab is FDA-approved for use in **Squamous Cell Carcinoma of the Head and Neck (SCCHN)**. It is used in combination with radiotherapy for locally advanced disease or as a palliative monotherapy/combination therapy for recurrent or metastatic cases. It is also notably used in **metastatic colorectal cancer**, provided the tumor is **KRAS wild-type**. **2. Why other options are incorrect:** * **Anal canal carcinoma:** The standard of care (Nigro protocol) involves Mitomycin and 5-Fluorouracil (5-FU) with radiation. Cetuximab is not a primary indication here. * **Gastric carcinoma:** First-line targeted therapy usually involves **Trastuzumab** (for HER2-positive cases) or **Ramucirumab** (VEGFR2 antagonist). * **Lung carcinoma:** While EGFR mutations are common in Non-Small Cell Lung Cancer (NSCLC), the preferred agents are **Tyrosine Kinase Inhibitors (TKIs)** like Erlotinib, Gefitinib, or Osimertinib, rather than Cetuximab. **High-Yield Clinical Pearls for NEET-PG:** * **Dermatologic Toxicity:** The most common side effect is an **acneiform skin rash**. Interestingly, the severity of the rash often correlates with a *positive* therapeutic response. * **Genetic Testing:** Before starting Cetuximab in colorectal cancer, testing for **KRAS mutations** is mandatory. If a KRAS mutation is present, Cetuximab will be ineffective because the pathway is "turned on" downstream of the receptor. * **Hypomagnesemia:** Cetuximab can cause significant magnesium wasting, requiring monitoring of electrolytes.

Question 392: Which of the following is an antifolate cancer drug?

A. Methotrexate (Correct Answer)
B. Azathioprine
C. Cyclosporin
D. Vincristine

Explanation: ### Explanation **Correct Option: A. Methotrexate** Methotrexate is the prototypical **antifolate** antimetabolite. It acts by competitively inhibiting the enzyme **Dihydrofolate Reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate (THF), the active form of folic acid required for the synthesis of thymidylate and purines. Consequently, DNA synthesis is halted, leading to "thymineless death" of rapidly dividing cancer cells. **Analysis of Incorrect Options:** * **B. Azathioprine:** This is a **purine analog** (a prodrug of 6-mercaptopurine). While it is an antimetabolite used as an immunosuppressant, it does not target folate metabolism. * **C. Cyclosporin:** This is a **calcineurin inhibitor**. It acts by inhibiting T-cell activation via the suppression of IL-2 production. It is not a cytotoxic anticancer drug but an immunosuppressant. * **D. Vincristine:** This is a **Vinca alkaloid** that acts as a mitotic inhibitor. It binds to tubulin and prevents microtubule polymerization, arresting the cell cycle in the M-phase. **High-Yield Clinical Pearls for NEET-PG:** * **Rescue Therapy:** High-dose Methotrexate toxicity is managed with **Leucovorin (Folinic acid)**, which bypasses the inhibited DHFR enzyme to provide a source of active folate. * **Adverse Effects:** Notable for causing **mucositis**, bone marrow suppression, and nephrotoxicity (due to crystalluria). * **Resistance:** Often occurs due to decreased drug uptake or increased synthesis of the DHFR enzyme. * **Other Antifolates:** Pemetrexed and Pralatrexate are newer agents in this class.

Question 393: All the following drugs are used in the treatment of metastatic breast cancer except?

A. Ixabepilone
B. Abemaciclib
C. Ribociclib
D. Sunitinib (Correct Answer)

Explanation: **Explanation:** The correct answer is **Sunitinib**. **1. Why Sunitinib is the correct answer:** Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor (TKI) that primarily inhibits VEGF receptors, PDGF receptors, and c-KIT [2]. It is the standard of care for **Metastatic Renal Cell Carcinoma (mRCC)**, Gastrointestinal Stromal Tumors (GIST), and Pancreatic Neuroendocrine Tumors (pNETs) [2]. It has no established role or FDA approval for the treatment of metastatic breast cancer. **2. Analysis of incorrect options:** * **Ixabepilone:** An **Epothilone B analog** that stabilizes microtubules (similar to taxanes but binds to a different site). It is specifically indicated for metastatic or locally advanced breast cancer, especially in patients resistant to anthracyclines and taxanes. * **Abemaciclib & Ribociclib:** These are **CDK 4/6 inhibitors**. They inhibit the cell cycle transition from G1 to S phase. Both are first-line treatments for Hormone Receptor (HR)-positive, HER2-negative metastatic breast cancer, usually in combination with aromatase inhibitors (e.g., Letrozole). **3. High-Yield Clinical Pearls for NEET-PG:** * **CDK 4/6 Inhibitors:** Palbociclib, Ribociclib, and Abemaciclib. *Mnemonic: "PAR" for Breast Cancer.* * **Ixabepilone:** Unique because it remains active in cells that overexpress P-glycoprotein (MDR1 gene), making it effective in taxane-resistant breast cancer. * **Sunitinib Side Effect:** Characteristically causes **Hand-Foot Syndrome** and yellowing of the skin/depigmentation of hair. * **Trastuzumab/Pertuzumab:** Targeted therapy for HER2-positive breast cancer [1], [2].

Question 394: All of the following statements about vincristine are true EXCEPT:

A. It is cell cycle specific and kills cells in the M phase.
B. Its toxicity primarily affects peripheral nerves and bone marrow.
C. Folic acid is not used to reverse its toxic effects.
D. It is a drug of choice for choriocarcinoma. (Correct Answer)

Explanation: **Explanation:** The correct answer is **D** because **Methotrexate** (a folate antagonist), not Vincristine, is the drug of choice for gestational choriocarcinoma. While Vincristine is used in various combination regimens for solid tumors and leukemias [2], it does not hold primary status for choriocarcinoma. **Analysis of Options:** * **Option A (True):** Vincristine is a **cell cycle-specific (CCS)** agent [1]. It binds to tubulin and inhibits its polymerization into microtubules, preventing the formation of the mitotic spindle [1]. This causes cell cycle arrest specifically in the **M phase (Mitosis)** [1]. * **Option B (False statement/True fact):** This is a tricky distractor. While Vincristine is famous for being **"bone marrow sparing"** (unlike Vinblastine) [3], it can still cause mild marrow suppression in some cases [3]. However, its **dose-limiting toxicity is peripheral neuropathy** (paresthesia, loss of reflexes, foot drop) [2], [3]. * **Option C (True):** Folic acid (Leucovorin) is used to "rescue" cells from Methotrexate toxicity. It has no biochemical role in reversing the microtubule inhibition caused by Vincristine. **Clinical Pearls for NEET-PG:** * **Vinca Alkaloids Mnemonic:** **V**incristine = **V**ery little marrow effect (Neurotoxicity); **V**inblastine = **B**lasts the **B**one marrow (Myelosuppression) [3]. * **Fatal Route:** Vincristine is for **Intravenous use ONLY**. Intrathecal administration is fatal due to ascending myeloencephalopathy. * **Syndrome of Inappropriate ADH (SIADH):** Vincristine is a well-known cause of drug-induced SIADH.

Question 395: For which condition is the drug Bozoib used?

A. Multiple myeloma (Correct Answer)
B. Renal cell carcinoma
C. Hepatocellular carcinoma
D. Pancreatic carcinoma

Explanation: **Explanation:** **Bortezomib** (often referred to in shorthand or slightly modified names in exams) is a first-in-class **proteasome inhibitor**. It specifically targets the **26S proteasome** complex, leading to the inhibition of the degradation of pro-apoptotic proteins and the stabilization of **NF-κB** inhibitors (IκB). In malignant plasma cells, this results in the induction of apoptosis and inhibition of cell survival pathways. * **Why Multiple Myeloma is correct:** Multiple myeloma cells are highly dependent on the proteasome system to clear the excessive amounts of abnormal immunoglobulins (M-proteins) they produce. By blocking the proteasome, Bortezomib causes "proteotoxic stress" and unfolded protein responses, making it a cornerstone therapy for both newly diagnosed and relapsed **Multiple Myeloma**, as well as Mantle Cell Lymphoma. * **Why other options are incorrect:** * **Renal Cell Carcinoma (RCC):** Primarily treated with Tyrosine Kinase Inhibitors (TKIs) like Sunitinib or mTOR inhibitors like Everolimus. * **Hepatocellular Carcinoma (HCC):** The standard systemic therapy involves multikinase inhibitors like **Sorafenib** or Lenvatinib. * **Pancreatic Carcinoma:** Typically managed with cytotoxic regimens like Gemcitabine or FOLFIRINOX. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Reversible inhibition of the 26S proteasome. * **Key Side Effect:** **Peripheral Neuropathy** (often dose-limiting). * **Viral Reactivation:** It significantly increases the risk of **Herpes Zoster** reactivation; therefore, patients are often started on prophylactic Acyclovir. * **Route:** Subcutaneous administration is preferred over intravenous to reduce the incidence of neuropathy.

Question 396: What is the most common dose-limiting toxicity of chemotherapeutic agents?

A. Myelosuppression (Correct Answer)
B. Gastrointestinal toxicity
C. Neurotoxicity
D. Alopecia

Explanation: **Explanation:** The most common dose-limiting toxicity (DLT) for the majority of cytotoxic chemotherapeutic agents is **Myelosuppression** (Bone Marrow Suppression). **Why Myelosuppression is the Correct Answer:** Cytotoxic drugs primarily target rapidly dividing cells by interfering with DNA synthesis or mitosis. Since the hematopoietic stem cells in the bone marrow have a high turnover rate, they are highly susceptible to these agents. This results in leucopenia (specifically neutropenia), thrombocytopenia, and anemia. Neutropenia is the most critical component, as it predisposes patients to life-threatening opportunistic infections, often necessitating dose reduction or treatment delay. **Analysis of Incorrect Options:** * **B. Gastrointestinal Toxicity:** While nausea, vomiting, and mucositis are very common side effects, they are usually manageable with antiemetics (like Ondansetron) and are rarely the primary factor that limits the maximum tolerated dose (except for specific drugs like Irinotecan or 5-FU). * **C. Neurotoxicity:** This is a specific DLT for certain classes (e.g., Vinca alkaloids like Vincristine, Taxanes, and Cisplatin) but is not the "most common" across the entire spectrum of chemotherapy. * **D. Alopecia:** Hair loss is a distressing side effect due to the high mitotic index of hair follicles, but it is cosmetic and never dose-limiting. **High-Yield Clinical Pearls for NEET-PG:** * **Exceptions:** Drugs that are **NOT** typically myelosuppressive include **Vincristine, Bleomycin, Cisplatin, and L-Asparaginase.** * **Nadir:** The point of lowest blood cell count after chemo, usually occurring 7–14 days post-treatment. * **Specific DLTs to remember:** * Cisplatin: Nephrotoxicity (prevented by aggressive hydration/Amifostine). * Doxorubicin: Cardiotoxicity (prevented by Dexrazoxane). * Bleomycin: Pulmonary Fibrosis. * Cyclophosphamide: Hemorrhagic Cystitis (prevented by MESNA).

Question 397: Erlotinib is used in which of the following cancers?

A. Colon cancer
B. Pancreatic cancer (Correct Answer)
C. Gall bladder cancer
D. GIST

Explanation: **Explanation:** **Erlotinib** is a small-molecule **Tyrosine Kinase Inhibitor (TKI)** that specifically targets the **Epidermal Growth Factor Receptor (EGFR/HER1)**. By inhibiting the intracellular phosphorylation of EGFR, it prevents the downstream signaling pathways responsible for cell proliferation and survival. **Why Pancreatic Cancer is correct:** Erlotinib is FDA-approved for use in combination with **Gemcitabine** as a first-line treatment for patients with locally advanced, unresectable, or metastatic **pancreatic cancer**. It is also a primary treatment for Non-Small Cell Lung Cancer (NSCLC), particularly in patients with specific EGFR mutations (Exon 19 deletions or Exon 21 L858R mutations). **Analysis of Incorrect Options:** * **A. Colon cancer:** The primary EGFR inhibitors used here are monoclonal antibodies like **Cetuximab** and **Panitumumab** (effective only in KRAS wild-type patients), not Erlotinib. * **C. Gall bladder cancer:** While research is ongoing, Erlotinib is not a standard-of-care or first-line therapy for biliary tract cancers. * **D. GIST (Gastrointestinal Stromal Tumor):** The drug of choice is **Imatinib**, which targets the **c-KIT** (CD117) tyrosine kinase, not EGFR. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** The most characteristic side effect of Erlotinib is an **acneiform skin rash**. Interestingly, the severity of the rash often correlates with a better therapeutic response. * **Metabolism:** It is metabolized by **CYP3A4**; therefore, smokers may require higher doses as smoking induces the metabolism of Erlotinib. * **Comparison:** Unlike Erlotinib (TKI), **Cetuximab** is a monoclonal antibody against EGFR. Both are distinct from **Trastuzumab**, which targets **HER2/neu**.

Question 398: Which of the following drugs is most emetogenic?

A. Cisplatin (Correct Answer)
B. Carboplatin
C. High dose cyclophosphamide
D. High dose methotrexate

Explanation: **Explanation:** The emetogenic potential of chemotherapy is categorized into four levels: High (>90% risk), Moderate (30–90%), Low (10–30%), and Minimal (<10%). **Cisplatin** is the classic prototype of a **highly emetogenic** drug. It induces nausea and vomiting through two mechanisms: 1. **Acute phase:** Release of serotonin (5-HT) from enterochromaffin cells in the GI tract, stimulating the 5-HT3 receptors. 2. **Delayed phase:** Activation of Neurokinin-1 (NK1) receptors by Substance P in the brainstem. Because Cisplatin has a >90% risk of emesis, it requires triple antiemetic therapy (5-HT3 antagonist + Dexamethasone + NK1 antagonist like Aprepitant). **Analysis of Incorrect Options:** * **Carboplatin:** While related to cisplatin, it is significantly less emetogenic and falls into the **Moderate** risk category. * **High-dose Cyclophosphamide:** Doses >1500 mg/m² are considered highly emetogenic, but **Cisplatin remains the gold standard** for the highest emetic risk in pharmacological comparisons. * **High-dose Methotrexate:** This is generally classified as having **Moderate** emetogenic potential. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of choice for Cisplatin-induced vomiting:** 5-HT3 antagonists (e.g., Ondansetron) for acute; NK1 antagonists (e.g., Aprepitant) for delayed. * **Other Highly Emetogenic Drugs:** Dacarbazine, Mechlorethamine, and high-dose Anthracyclines (Doxorubicin). * **Least Emetogenic (Minimal risk):** Vincristine, Vinblastine, and Bleomycin. * **Cisplatin Toxicity Profile:** Remember the mnemonic "3 N's" — **N**ephrotoxicity (prevented by Amifostine/hydration), **N**eurotoxicity (ototoxicity), and **N**ausea/vomiting.

Question 399: Bicalutamide is a specific inhibitor of which of the following?

A. 5-alpha reductase
B. Androgen receptors (Correct Answer)
C. Aromatase
D. Estrogen receptor

Explanation: **Explanation:** **Bicalutamide** is a potent, non-steroidal **Androgen Receptor (AR) antagonist**. It works by competitively inhibiting the binding of dihydrotestosterone (DHT) and testosterone to androgen receptors in target tissues, such as the prostate gland. By blocking these receptors, it prevents the growth-stimulating effects of androgens on prostate cancer cells. **Analysis of Options:** * **Option B (Correct):** Bicalutamide belongs to the "lutamide" family (including Flutamide and Enzalutamide), which are pure anti-androgens used primarily in the management of metastatic **Prostate Carcinoma**. * **Option A (Incorrect):** Inhibitors of 5-alpha reductase include **Finasteride** and **Dutasteride**. These drugs prevent the conversion of testosterone to the more potent DHT and are used for Benign Prostatic Hyperplasia (BPH) and alopecia. * **Option C (Incorrect):** Aromatase inhibitors include **Anastrozole**, **Letrozole**, and **Exemestane**. They block the conversion of androgens to estrogens and are used in postmenopausal breast cancer. * **Option D (Incorrect):** Estrogen receptor antagonists/modulators include **Tamoxifen** (SERM) and **Fulvestrant** (SERD), used primarily in breast cancer treatment. **High-Yield Clinical Pearls for NEET-PG:** * **Combined Androgen Blockade (CAB):** Bicalutamide is often used in combination with GnRH agonists (like Leuprolide) to prevent the **"testosterone flare"** (initial surge in testosterone) that occurs at the start of GnRH therapy. * **Advantages:** Compared to Flutamide, Bicalutamide has a longer half-life (allowing once-daily dosing) and a lower risk of hepatotoxicity. * **Side Effects:** Common side effects include gynecomastia, hot flashes, and hepatotoxicity (monitor LFTs).

Question 400: Pentostatin acts by inhibiting which enzyme?

A. RNA dependent DNA polymerase
B. Aldolase
C. Adenosine deaminase (Correct Answer)
D. Adenylyl cyclase

Explanation: **Explanation:** **Pentostatin** (2'-deoxycoformycin) is a potent transition-state analog inhibitor of the enzyme **Adenosine Deaminase (ADA)**. **Mechanism of Action:** ADA is a critical enzyme in the purine salvage pathway that converts adenosine to inosine and deoxyadenosine to deoxyinosine. By inhibiting ADA, Pentostatin leads to an intracellular accumulation of **deoxyadenosine triphosphate (dATP)**. High levels of dATP are toxic to lymphocytes because they inhibit ribonucleotide reductase, thereby depleting the deoxynucleotide pools required for DNA synthesis and repair. This leads to apoptosis, particularly in T and B cells. **Analysis of Incorrect Options:** * **A. RNA-dependent DNA polymerase:** Also known as Reverse Transcriptase, this is the target for antiretroviral drugs (like Zidovudine) used in HIV treatment, not Pentostatin. * **B. Aldolase:** This is a glycolytic enzyme. While some experimental drugs target metabolic pathways, it is not the target for any standard anticancer purine analog. * **D. Adenylyl cyclase:** This enzyme converts ATP to cyclic AMP (cAMP) and is involved in G-protein coupled receptor signaling. It is not a target for cytotoxic chemotherapy. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Pentostatin is highly effective and considered a primary treatment for **Hairy Cell Leukemia**. * **Toxicity:** The major dose-limiting toxicities are myelosuppression and nephrotoxicity. * **ADA Deficiency:** Congenital deficiency of Adenosine Deaminase leads to **Severe Combined Immunodeficiency (SCID)**, highlighting the enzyme's vital role in lymphocyte survival. * **Related Drug:** **Cladribine** is another purine analog used for Hairy Cell Leukemia; it is resistant to degradation by ADA.

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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