Anticancer Drugs Practice Questions

Q: Sorafenib, a tyrosine kinase inhibitor, is used to treat which of the following conditions?

Hepatocellular carcinoma. **Explanation:** **Sorafenib** is a multi-kinase inhibitor that targets several pathways involved in tumor growth and angiogenesis. It primarily inhibits **Raf serine/threonine kinases** (C-Raf, B-Raf) and **Receptor Tyrosine Kinases** (VEGFR-2, VEGFR-3, PDGFR-β). 1. **Why Hepatocellular Carcinoma (HCC) is correct:** Sorafenib was the first systemic therapy proven to extend survival in patients with advanced, unresectable HCC. By inhibiting the Raf/MEK/ERK pathway and blocking VEGF receptors, it effectively reduces tumor proliferation and angiogenesis in the highly vascular environment of the liver. It is also FDA-approved for advanced **Renal Cell Carcinoma (RCC)** and differentiated thyroid cancer. 2. **Why other options are incorrect:** * **Myeloproliferative disorders:** These are typically treated with **Imatinib** (CML - BCR-ABL inhibitor) or **Ruxolitinib** (Polycythemia Vera/Myelofibrosis - JAK2 inhibitor). * **Follicular lymphoma:** This is a B-cell malignancy usually managed with **Rituximab** (anti-CD20 monoclonal antibody) or alkylating agents. * **Medullary carcinoma thyroid:** While Sorafenib is used for *differentiated* thyroid cancer, the drugs of choice for Medullary thyroid cancer are **Vandetanib** or **Cabozantinib** (targeting the RET proto-oncogene). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Dual action (Antiproliferative via Raf + Anti-angiogenic via VEGFR/PDGFR). * **Key Side Effect:** **Hand-Foot Skin Reaction (HFSR)**—characterized by redness, pain, and hyperkeratosis on palms and soles (distinct from the Hand-Foot Syndrome caused by 5-FU). * **Other Multi-kinase Inhibitors:** **Sunitinib** (used in RCC and GIST) and **Erlotinib/Gefitinib** (EGFR inhibitors used in NSCLC).

Q: Which of the following is a cytoprotective agent against radiation-induced stomatitis?

Amifostine. **Explanation:** **Amifostine (Option A)** is the correct answer. It is a **cytoprotective adjuvant** (a prodrug) that is converted by alkaline phosphatase into an active free thiol metabolite. This metabolite acts as a potent scavenger of free radicals generated by ionizing radiation and certain chemotherapeutic agents (like Cisplatin). Because alkaline phosphatase activity is higher in normal tissues and the pH is more alkaline compared to the acidic tumor microenvironment, Amifostine selectively protects healthy cells. It is FDA-approved to reduce the incidence of **radiation-induced xerostomia (dry mouth)** and **stomatitis** in patients undergoing radiotherapy for head and neck cancer. **Analysis of Incorrect Options:** * **Metronidazole (Option B):** An antibiotic and antiprotozoal agent. While it can act as a radiosensitizer for hypoxic cells, it is not used as a cytoprotective agent against stomatitis. * **Misonidazole (Option C):** A known **radiosensitizer**. It mimics oxygen to increase the sensitivity of hypoxic tumor cells to radiation, making them easier to kill; it does not protect normal tissues. * **Acarbose (Option D):** An alpha-glucosidase inhibitor used in the management of Type 2 Diabetes Mellitus to reduce postprandial hyperglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **Amifostine** also protects against **Cisplatin-induced nephrotoxicity**. * **Mesna** is the cytoprotective agent used to prevent **hemorrhagic cystitis** caused by Cyclophosphamide or Ifosfamide. * **Dexrazoxane** is used to prevent **anthracycline-induced cardiotoxicity** (e.g., Doxorubicin). * **Leucovorin (Folinic acid)** is used as a "rescue" for **Methotrexate** toxicity.

Q: The MDR gene acts by which mechanism?

Causing efflux of drugs. **Explanation:** The **MDR-1 gene** (Multi-Drug Resistance gene 1) encodes for a cell surface glycoprotein known as **P-glycoprotein (P-gp)** [1]. This protein belongs to the ATP-binding cassette (ABC) transporter family [2]. **1. Why Option C is Correct:** The primary mechanism of the MDR-1 gene is the synthesis of P-glycoprotein, which acts as an **ATP-dependent efflux pump** [3]. It actively pumps various hydrophobic anticancer drugs (such as Vinca alkaloids, Anthracyclines, and Taxanes) out of the tumor cell [1]. This reduces the intracellular concentration of the drug to sub-therapeutic levels, leading to resistance. **2. Why Other Options are Incorrect:** * **Option A:** Blocking drug activation is a mechanism seen with drugs like **5-Fluorouracil** or **Cytarabine**, where the cell fails to convert the prodrug into its active metabolite. * **Option B:** Blocking DNA synthesis is the **mechanism of action** of antimetabolites (e.g., Methotrexate), not a mechanism of the MDR gene [4]. * **Option C:** Inhibiting DNA repair is a strategy used by certain drugs (like PARP inhibitors) to kill cancer cells; it is not the function of the MDR gene. **High-Yield Clinical Pearls for NEET-PG:** * **Drugs affected by MDR:** "VATP" — **V**inca alkaloids, **A**nthracyclines (Doxorubicin), **T**axanes (Paclitaxel), and **P**odophyllotoxins (Etoposide) [1]. * **Drugs NOT affected by MDR:** Alkylating agents (Cyclophosphamide) and Antimetabolites. * **P-gp Inhibitors:** Drugs like **Verapamil**, Quinidine, and Cyclosporine can inhibit P-glycoprotein and are sometimes studied to reverse drug resistance. * **Normal Location:** P-gp is also found in the Blood-Brain Barrier (BBB), liver, and kidneys, where it protects normal tissues from toxins [3].

Q: A 56-year-old female with lymph-node-positive breast cancer was treated with systemic chemotherapy. Four weeks later, she developed frequent urination, suprapubic pain, dysuria, and hematuria. Which of the following could have prevented this patient's condition?

Mesna. **Explanation:** The patient is presenting with **Hemorrhagic Cystitis**, a classic adverse effect associated with high-dose **Cyclophosphamide** or **Ifosfamide** therapy (alkylating agents commonly used in breast cancer regimens). These drugs are metabolized into **Acrolein**, a toxic metabolite that accumulates in the bladder, causing direct mucosal damage, inflammation, and bleeding. **Why Mesna is the correct answer:** **Mesna (2-Mercaptoethane sulfonate)** is a sulfhydryl compound that prevents hemorrhagic cystitis through two mechanisms: 1. It binds to and neutralizes acrolein in the urinary tract to form a non-toxic compound. 2. It slows the degradation of 4-hydroxy metabolites of cyclophosphamide. *Note: Vigorous hydration is also essential alongside Mesna.* **Analysis of Incorrect Options:** * **A. Folinic acid (Leucovorin):** Used as a "rescue" therapy to prevent bone marrow suppression after high-dose **Methotrexate** or to potentiate the action of 5-Fluorouracil. * **C. Dexrazoxane:** An iron-chelating agent used to prevent **Anthracycline-induced cardiotoxicity** (e.g., Doxorubicin). * **D. Amifostine:** A cytoprotective free-radical scavenger used to reduce **Cisplatin-induced nephrotoxicity** and xerostomia. **High-Yield Clinical Pearls for NEET-PG:** * **Acrolein** = The culprit for Hemorrhagic Cystitis. * **Mesna** = The specific antidote/preventative agent. * **Ifosfamide** is more urotoxic than Cyclophosphamide; therefore, Mesna is mandatory with Ifosfamide. * **Other uses of Cyclophosphamide:** Apart from cancer, it is used in Wegener’s Granulomatosis (GPA) and Nephrotic syndrome. Long-term risk includes Transitional Cell Carcinoma of the bladder.

Q: Imatinib mesylate is most useful in the treatment of which condition?

Chronic myeloid leukaemia. **Explanation:** **Imatinib mesylate** is the prototype of a class of drugs known as **Tyrosine Kinase Inhibitors (TKIs)**. It is considered the first-line treatment and the "gold standard" for **Chronic Myeloid Leukaemia (CML)**. **Why Option B is Correct:** The hallmark of CML is the **Philadelphia chromosome [t(9;22)]**, which creates the **BCR-ABL fusion gene**. This gene encodes a constitutively active tyrosine kinase protein that drives uncontrolled cellular proliferation. Imatinib works by competitively binding to the ATP-binding site of the BCR-ABL enzyme, inhibiting its activity and inducing apoptosis in leukemic cells. **Why Other Options are Incorrect:** * **A. Chronic Lymphoid Leukaemia (CLL):** The primary treatments involve agents like Fludarabine, Rituximab, or Ibrutinib (a BTK inhibitor), as CLL does not typically involve the BCR-ABL mutation. * **C. Acute Myeloid Leukaemia (AML):** Standard induction therapy is the "7+3" regimen (Cytarabine + Daunorubicin). Imatinib is only used in rare cases of Philadelphia chromosome-positive (Ph+) AML. * **D. Acute Lymphoid Leukaemia (ALL):** While Imatinib is used in **Ph+ ALL** (a specific subtype), it is not the primary treatment for the general category of ALL, which relies on multi-agent chemotherapy (Vincristine, Steroids, L-Asparaginase). **High-Yield Clinical Pearls for NEET-PG:** * **Other Indications:** Imatinib is also the drug of choice for **Gastrointestinal Stromal Tumors (GIST)** by inhibiting the **c-KIT** tyrosine kinase. * **Mechanism:** It is a selective inhibitor of BCR-ABL, c-KIT, and PDGFR. * **Side Effects:** The most characteristic side effect is **periorbital edema** (fluid retention). * **Resistance:** Resistance to Imatinib often occurs due to the **T315I mutation**, which requires newer TKIs like **Ponatinib**.

Q: What is the most common side effect of mycophenolate mofetil?

Diarrhea. **Explanation:** **Mycophenolate Mofetil (MMM)** is a potent immunosuppressant that acts by inhibiting **Inosine Monophosphate Dehydrogenase (IMPDH)**, the rate-limiting enzyme in the *de novo* synthesis of guanosine nucleotides. Since T and B lymphocytes lack the salvage pathway for purine synthesis, they are selectively inhibited. **1. Why Diarrhea is the Correct Answer:** Gastrointestinal (GI) disturbances are the most frequent adverse effects of MMF. Among these, **diarrhea** is the most common (occurring in up to 30-50% of patients), followed by nausea, vomiting, and abdominal pain. This occurs because MMF exerts a direct toxic effect on the rapidly dividing intestinal epithelial cells, which, like lymphocytes, are partially dependent on the *de novo* purine pathway. **2. Why Other Options are Incorrect:** * **Marrow suppression (A):** While MMF can cause leukopenia and anemia, it is generally considered less myelosuppressive than Azathioprine. GI toxicity remains more prevalent. * **Nephrotoxicity (B):** MMF is notably **non-nephrotoxic**. This is a major clinical advantage over Calcineurin Inhibitors (CNIs) like Cyclosporine and Tacrolimus. * **Glucose intolerance (C):** This is a classic side effect of Corticosteroids and Tacrolimus, not MMF. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Reversible inhibition of IMPDH. * **Clinical Use:** Prophylaxis of transplant rejection (often replacing Azathioprine) and treatment of Lupus Nephritis. * **Teratogenicity:** MMF is highly teratogenic (Category D); it is associated with **congenital malformations** (ear and facial defects). * **Drug Interaction:** Antacids containing magnesium or aluminum hydroxide decrease MMF absorption.

Q: Which of the following are alkylating agents?

Cyclophosphamide. **Explanation:** Alkylating agents are a class of cell cycle-nonspecific antineoplastic drugs that act by forming covalent bonds with DNA, specifically at the **N7 position of guanine**. This results in DNA cross-linking, strand breakage, and inhibition of DNA replication, ultimately leading to cell death (apoptosis). **Why Cyclophosphamide is correct:** **Cyclophosphamide** is a nitrogen mustard and a classic example of an alkylating agent. It is a prodrug activated in the liver by cytochrome P450 enzymes into its active forms, phosphoramide mustard and acrolein. It is widely used in treating lymphomas, leukemias, and solid tumors. **Analysis of Incorrect Options:** * **A. Vincristine:** This is a **Vinca alkaloid** (Antimitotic). It works by binding to tubulin and inhibiting microtubule polymerization, causing cell cycle arrest in the M-phase. * **B. Actinomycin-D (Dactinomycin):** This is an **Antitumor Antibiotic**. It acts by intercalating between DNA base pairs and inhibiting RNA synthesis by blocking RNA polymerase. * **C. Chlorambucil:** While Chlorambucil **is** also an alkylating agent (nitrogen mustard), in the context of single-choice NEET-PG questions, Cyclophosphamide is often the "most representative" or intended answer if only one can be selected. *Note: If this were a multiple-response question, both C and D would be correct.* **High-Yield Clinical Pearls for NEET-PG:** * **Acrolein Toxicity:** The metabolite acrolein causes **Hemorrhagic Cystitis**. This is prevented by aggressive hydration and the administration of **MESNA** (a sulfhydryl compound that neutralizes acrolein). * **Other Alkylating Agents:** Busulfan (causes pulmonary fibrosis), Nitrosoureas (Carmustine/Lomustine - cross the BBB), and Dacarbazine. * **Resistance:** Often occurs due to increased production of glutathione or enhanced DNA repair mechanisms (e.g., MGMT enzyme).

Q: Which of the following antineoplastic drugs is known to cause pulmonary toxicity?

Bleomycin. **Explanation:** **Bleomycin (Option A)** is the correct answer. It is a cytotoxic antibiotic that acts by generating free radicals, which cause oxidative damage and double-stranded breaks in DNA. The primary dose-limiting toxicity of Bleomycin is **pulmonary fibrosis**. This occurs because the lungs lack the enzyme **bleomycin hydrolase**, which normally inactivates the drug. Without this enzyme, the drug accumulates in lung tissue, leading to inflammation and eventual fibrosis. **Why other options are incorrect:** * **5-Fluorouracil (Option B):** An antimetabolite primarily known for causing gastrointestinal toxicity (mucositis, diarrhea) and **Hand-Foot Syndrome** (palmar-plantar erythrodysesthesia). * **Cisplatin (Option C):** A platinum compound notorious for **nephrotoxicity** and **ototoxicity**. It is also highly emetogenic. * **Vincristine (Option D):** A vinca alkaloid that inhibits microtubule assembly. Its hallmark toxicity is **peripheral neuropathy** (paresthesia, loss of reflexes) and autonomic dysfunction (constipation). Notably, it is "bone marrow sparing." **High-Yield Clinical Pearls for NEET-PG:** 1. **Monitoring:** Patients on Bleomycin should undergo regular **Pulmonary Function Tests (PFTs)**; a decrease in DLCO (Diffusing capacity of the lungs for carbon monoxide) is an early sign of toxicity. 2. **Oxygen Warning:** Patients with a history of Bleomycin use are at high risk of severe lung injury if exposed to high concentrations of inspired oxygen (e.g., during surgery). 3. **Busulfan:** Another high-yield drug associated with "Busulfan Lung" (interstitial fibrosis). 4. **Skin Toxicity:** Bleomycin can also cause **flagellate hyperpigmentation** of the skin.

Q: Which of the following is an adenosine deaminase inhibitor?

Pentostatin. **Explanation:** **1. Correct Answer: Pentostatin** Pentostatin (2'-deoxycoformycin) is a potent, irreversible inhibitor of the enzyme **Adenosine Deaminase (ADA)**. ADA is essential for the purine salvage pathway, converting adenosine to inosine and deoxyadenosine to deoxyinosine. Inhibition of ADA leads to the toxic accumulation of intracellular deoxyadenosine triphosphate (dATP). High levels of dATP inhibit ribonucleotide reductase, thereby stalling DNA synthesis and inducing apoptosis, particularly in lymphocytes. It is the drug of choice for **Hairy Cell Leukemia**. **2. Analysis of Incorrect Options:** * **TxA2 (Thromboxane A2):** This is a lipid signaling molecule (eicosanoid) produced by platelets. It promotes platelet aggregation and vasoconstriction. It is not an anticancer drug or an enzyme inhibitor in this context. * **Cladribine:** While also used for Hairy Cell Leukemia, Cladribine is a **purine nucleoside analog** (resistant to degradation by ADA). It mimics adenosine and incorporates into DNA, causing strand breaks. It does not inhibit the ADA enzyme itself. * **All of the above:** Incorrect, as only Pentostatin fits the specific mechanism of ADA inhibition. **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Both Pentostatin and Cladribine are highly effective for Hairy Cell Leukemia, but their mechanisms differ (Pentostatin = ADA inhibitor; Cladribine = Purine analog). * **ADA Deficiency:** Congenital deficiency of Adenosine Deaminase leads to **SCID (Severe Combined Immunodeficiency)** due to the accumulation of dATP, which is toxic to T and B cells. * **Other Purine Analogs:** Remember **Fludarabine** (used in CLL) and **6-Mercaptopurine** (inhibits PRPP amidotransferase).

Question 1

Sorafenib, a tyrosine kinase inhibitor, is used to treat which of the following conditions?

Accepted Answer

Hepatocellular carcinoma

Answer

Myeloproliferative disorder

Answer

Follicular lymphoma

Answer

Medullary carcinoma thyroid

Question 2

Which of the following is a cytoprotective agent against radiation-induced stomatitis?

Accepted Answer

Amifostine

Answer

Metronidazole

Answer

Misonidazole

Answer

Acarbose

Question 3

The MDR gene acts by which mechanism?

Accepted Answer

Causing efflux of drugs

Answer

Blocking drug activation

Answer

Blocking intracellular DNA synthesis

Answer

Inhibiting DNA repair

Question 4

A 56-year-old female with lymph-node-positive breast cancer was treated with systemic chemotherapy. Four weeks later, she developed frequent urination, suprapubic pain, dysuria, and hematuria. Which of the following could have prevented this patient's condition?

Accepted Answer

Mesna

Answer

Folinic acid

Answer

Dexrazoxane

Answer

Amifostine

Question 5

Imatinib mesylate is most useful in the treatment of which condition?

Accepted Answer

Chronic myeloid leukaemia

Answer

Chronic lymphoid leukaemia

Answer

Acute myeloid leukaemia

Answer

Acute lymphoid leukaemia

Question 6

What is the most common side effect of mycophenolate mofetil?

Accepted Answer

Diarrhea

Answer

Marrow suppression

Answer

Nephrotoxicity

Answer

Glucose intolerance

Question 7

Which of the following are alkylating agents?

Accepted Answer

Cyclophosphamide

Answer

Vincristine

Answer

Actinomycin-D

Answer

Chlorambucil

Question 8

Which of the following antineoplastic drugs is known to cause pulmonary toxicity?

Accepted Answer

Bleomycin

Answer

5-fluorouracil

Answer

Cisplatin

Answer

Vincristine

Question 9

Which of the following is an adenosine deaminase inhibitor?

Accepted Answer

Pentostatin

Answer

TxA2

Answer

Cladribine

Answer

All of the above

Question 10

Imatinib is used in the treatment of which condition?

Accepted Answer

Chronic Myeloid Leukemia (CML)

Answer

Myelodysplastic Syndromes (MDS)

Answer

Acute Lymphoblastic Leukemia (ALL)

Answer

All of the above

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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