Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 91: Which anticancer drug is known to cause cerebellar ataxia?

A. Cyclophosphamide
B. Chloramphenicol
C. Cytarabine (Correct Answer)
D. Vinblastine

Explanation: **Explanation:** **Cytarabine (Ara-C)** is the correct answer. It is a pyrimidine analog that inhibits DNA polymerase. The occurrence of **cerebellar ataxia** (dysarthria, nystagmus, and gait instability) is a classic, dose-limiting neurotoxicity associated specifically with **high-dose Cytarabine therapy**. This occurs because the drug can cross the blood-brain barrier and cause direct damage to **Purkinje cells** in the cerebellum. Risk factors include renal impairment (due to decreased clearance of the metabolite Ara-U) and older age. **Analysis of Incorrect Options:** * **Cyclophosphamide:** An alkylating agent primarily known for **hemorrhagic cystitis** (prevented by Mesna) and bone marrow suppression. It does not typically cause cerebellar toxicity. * **Chloramphenicol:** This is an antibiotic, not a primary anticancer drug. Its hallmark toxicities are **Gray Baby Syndrome** and dose-dependent/idiosyncratic bone marrow suppression (aplastic anemia). * **Vinblastine:** A Vinca alkaloid that inhibits microtubule assembly. Its primary toxicity is **bone marrow suppression** ("Blastine blasts the marrow"), whereas its sister drug, Vincristine, is more famous for peripheral neuropathy, not cerebellar ataxia. **High-Yield Clinical Pearls for NEET-PG:** * **Cytarabine:** Remember the "3 Cs": **C**ytarabine, **C**erebellar ataxia, and **C**onjunctivitis (chemical conjunctivitis is another high-dose side effect). * **Monitoring:** Patients on high-dose Ara-C must perform daily "finger-to-nose" tests and handwriting checks to screen for early signs of ataxia. * **Drug of Choice:** Cytarabine is a cornerstone in the induction therapy of **Acute Myeloid Leukemia (AML)**.

Question 92: Which of the following anti-cancer drugs is a monoclonal antibody?

A. Di-ethyl-stilbesterol
B. Tamoxifen
C. Rituximab (Correct Answer)
D. Bortezomib

Explanation: ### Explanation **Correct Answer: C. Rituximab** **1. Why Rituximab is correct:** Rituximab is a **chimeric monoclonal antibody (mAb)** directed against the **CD20 antigen**, which is primarily found on the surface of B-lymphocytes. By binding to CD20, it induces B-cell lysis through antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity. It is a cornerstone therapy for B-cell non-Hodgkin lymphomas, Chronic Lymphocytic Leukemia (CLL), and autoimmune conditions like Rheumatoid Arthritis. **2. Why the other options are incorrect:** * **A. Di-ethyl-stilbesterol (DES):** This is a **synthetic non-steroidal estrogen**. Historically used for prostate cancer, it is now largely obsolete due to its side effect profile (e.g., thromboembolism and clear cell adenocarcinoma in daughters of treated women). * **B. Tamoxifen:** This is a **Selective Estrogen Receptor Modulator (SERM)**. It acts as an antagonist in breast tissue and is the gold standard for hormone-receptor-positive breast cancer. * **C. Bortezomib:** This is a **Proteasome Inhibitor**. It inhibits the 26S proteasome, leading to the buildup of pro-apoptotic proteins. It is a first-line agent for Multiple Myeloma. **3. High-Yield Clinical Pearls for NEET-PG:** * **Nomenclature Tip:** Drugs ending in **"-mab"** are Monoclonal Antibodies; those ending in **"-nib"** are small molecule Kinase Inhibitors (e.g., Imatinib). * **Rituximab Side Effect:** The most significant acute side effect is an **infusion-related reaction** (cytokine release syndrome). Pre-medication with antihistamines and acetaminophen is required. * **Screening:** Always screen for **Hepatitis B** before starting Rituximab, as it can cause viral reactivation. * **Other common mAbs:** Trastuzumab (HER2/neu), Bevacizumab (VEGF), Cetuximab (EGFR).

Question 93: Which of the following is a proliferation signal inhibitor?

A. Tacrolimus
B. Sirolimus (Correct Answer)
C. Cyclosporine
D. None of the above

Explanation: **Explanation:** The correct answer is **Sirolimus (Rapamycin)**. **1. Why Sirolimus is the Proliferation Signal Inhibitor:** Sirolimus belongs to the class of drugs known as **mTOR (mammalian Target of Rapamycin) inhibitors**. Its mechanism involves binding to the intracellular protein **FKBP-12**. This complex then inhibits the mTOR enzyme, which is a critical serine-threonine kinase. mTOR is responsible for regulating the cell cycle; its inhibition blocks the response to Interleukin-2 (IL-2), thereby arresting the cell cycle in the **G1 to S phase**. Because it stops the "signal" that leads to T-cell proliferation rather than just inhibiting cytokine production, it is classified as a **Proliferation Signal Inhibitor (PSI)**. **2. Why the other options are incorrect:** * **Tacrolimus (Option A) and Cyclosporine (Option C):** These are **Calcineurin Inhibitors (CNIs)**. They work upstream of Sirolimus by inhibiting the phosphatase calcineurin. This prevents the dephosphorylation of NFAT (Nuclear Factor of Activated T-cells), which is required for the *transcription* of IL-2. They inhibit the **production** of signals, whereas Sirolimus inhibits the **response** to the signal. **3. NEET-PG High-Yield Pearls:** * **Side Effects:** Unlike CNIs, Sirolimus is **not nephrotoxic**. Its primary side effects are hyperlipidemia (hypertriglyceridemia), thrombocytopenia, and impaired wound healing. * **Clinical Use:** Sirolimus is used in organ transplantation and is also used in **drug-eluting stents** (to prevent neointimal hyperplasia/restenosis). * **Everolimus:** A closely related mTOR inhibitor with a shorter half-life. * **Mnemonic:** Sirolimus **S**pares the kidney (Non-nephrotoxic) and stops the **S**ignal (PSI).

Question 94: Study light is caused by?

A. Vinca alkaloids
B. Alkylation agents (Correct Answer)
C. Antimetabolite
D. Antinomycin D

Explanation: **Explanation:** The term **"Study Light"** refers to a specific clinical phenomenon associated with the administration of **Alkylating agents**, most notably **Nitrogen Mustards** (like Mechlorethamine). ### 1. Why Alkylating Agents are Correct: When alkylating agents are administered intravenously, they can cause **phlebitis** (inflammation of the vein) and localized skin reactions. Patients often report seeing a **"blue-ish light"** or a "flash of light" during the infusion, or they may develop a characteristic **hyperpigmentation** along the track of the vein used for injection. This streaky, linear hyperpigmentation is colloquially referred to as "Study Light" or "Serpentine Supra-venous Hyperpigmentation." It is a high-yield dermatological side effect specific to this class. ### 2. Why Other Options are Incorrect: * **Vinca Alkaloids (e.g., Vincristine):** These are potent vesicants. If they extravasate, they cause severe tissue necrosis and cellulitis, but they are not associated with the "Study Light" phenomenon. Their primary dose-limiting toxicity is peripheral neuropathy. * **Antimetabolites (e.g., Methotrexate, 5-FU):** While 5-Fluorouracil (5-FU) can also cause serpentine hyperpigmentation, the classic association for the specific term "Study Light" in pharmacological literature is linked to alkylating agents. * **Actinomycin D:** This is an antitumor antibiotic known for causing "Radiation Recall" (skin inflammation at sites of previous radiation) and being a severe vesicant, but it does not produce the study light effect. ### 3. NEET-PG High-Yield Pearls: * **Serpentine Supra-venous Hyperpigmentation:** Most commonly caused by **5-Fluorouracil**, **Mechlorethamine**, and **Docetaxel**. * **Vincristine Side Effect:** "Glove and stocking" anesthesia and paralytic ileus. * **Cyclophosphamide (Alkylating agent):** Causes Hemorrhagic Cystitis (prevented by **MESNA**). * **Busulfan (Alkylating agent):** Causes Pulmonary Fibrosis and "Busulfan Tan" (generalized hyperpigmentation).

Question 95: Siltuximab is used in the treatment of which condition?

A. Castleman disease (Correct Answer)
B. Sézary syndrome
C. Ankylosing spondylitis
D. Non-Hodgkin lymphoma

Explanation: **Explanation:** **Siltuximab** is a chimeric monoclonal antibody that acts as an **Interleukin-6 (IL-6) antagonist**. It binds directly to soluble IL-6, preventing it from binding to its receptors. 1. **Why Option A is Correct:** **Castleman disease** (specifically Multicentric Castleman Disease or MCD) is a rare lymphoproliferative disorder characterized by the overproduction of IL-6. This cytokine excess leads to systemic inflammation, lymphadenopathy, and organ dysfunction. Siltuximab is the FDA-approved first-line therapy for patients with MCD who are HIV-negative and HHV-8-negative, as it neutralizes the driver of the disease. 2. **Why Other Options are Incorrect:** * **B. Sézary syndrome:** This is a leukemic form of cutaneous T-cell lymphoma. Treatment typically involves photopheresis, retinoids (Bexarotene), or Mogamulizumab (anti-CCR4). * **C. Ankylosing spondylitis:** This is an inflammatory arthritis treated with NSAIDs, TNF-inhibitors (Etanercept, Adalimumab), or IL-17 inhibitors (Secukinumab). * **D. Non-Hodgkin lymphoma:** Treatment usually involves the CHOP regimen and anti-CD20 antibodies like **Rituximab**. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Siltuximab binds to **IL-6**, whereas **Tocilizumab** and **Sarilumab** bind to the **IL-6 Receptor**. * **Indication:** Specifically used for **MCD** (Multicentric Castleman Disease). * **Side Effects:** Upper respiratory tract infections, pruritus, and hyperuricemia. * **IL-6 Connection:** Remember that IL-6 is also a key mediator in the pathogenesis of Rheumatoid Arthritis and the Cytokine Release Syndrome (CRS) seen in CAR-T cell therapy.

Question 96: All of the following are true about paclitaxel except?

A. Stabilizes microtubules and prevents polymerization
B. Used in ovarian, cervix, and breast cancer
C. Most commonly causes myelosuppression and alopecia
D. Obtained from E. coli (Correct Answer)

Explanation: **Explanation:** **Why Option D is the Correct Answer (The Exception):** Paclitaxel is a **natural product**, not a recombinant protein derived from bacteria. It was originally isolated from the bark of the **Pacific Yew tree (*Taxus brevifolia*)**. Modern production primarily utilizes semi-synthetic processes starting from precursors found in the needles of the European Yew (*Taxus baccata*). Drugs obtained from *E. coli* are typically recombinant proteins like L-asparaginase or insulin, making this statement false. **Analysis of Other Options:** * **Option A:** This describes the unique mechanism of action of Taxanes. Unlike Vinca alkaloids (which prevent polymerization), Paclitaxel **binds to the β-tubulin subunit**, promoting and **stabilizing microtubule assembly**. This prevents depolymerization, freezing the cell in the M-phase (mitotic spindle poison). * **Option B:** Paclitaxel is a broad-spectrum agent. It is a first-line treatment for **ovarian cancer** (often with Carboplatin) and is highly effective in advanced **breast, lung, and cervical cancers**. * **Option C:** **Myelosuppression** (specifically neutropenia) is the dose-limiting toxicity. **Alopecia** is almost universal with taxane therapy. **NEET-PG High-Yield Pearls:** * **Adverse Effect:** Paclitaxel is formulated in Cremophor EL, which often causes **hypersensitivity reactions**. Pre-treatment with dexamethasone and H1/H2 blockers is mandatory. * **Nab-paclitaxel:** An albumin-bound formulation that reduces hypersensitivity risks. * **Neurotoxicity:** Peripheral neuropathy (stocking-glove pattern) is a common side effect. * **Mnemonic:** "Taxanes **T**ighten the microtubules; Vincas **V**aporize them."

Question 97: Melphalan is used in which of the following conditions?

A. Multiple myeloma (Correct Answer)
B. Wilm's tumour
C. Neuroblastoma
D. Retinoblastoma

Explanation: **Explanation:** **Melphalan** is a nitrogen mustard derivative and a potent **alkylating agent**. It works by forming covalent bonds with DNA, specifically at the N7 position of guanine, leading to DNA cross-linking and subsequent apoptosis of rapidly dividing cells [1]. 1. **Why Multiple Myeloma is correct:** Melphalan is a cornerstone in the treatment of **Multiple Myeloma** [2]. It is used both in standard chemotherapy regimens (often combined with Prednisone) and in high doses as a conditioning agent prior to **Autologous Stem Cell Transplantation (ASCT)**. Its high efficacy against plasma cells makes it the drug of choice for this condition. 2. **Why other options are incorrect:** * **Wilm’s Tumour:** Primarily treated with a combination of Actinomycin D, Vincristine, and sometimes Doxorubicin. * **Neuroblastoma:** Management typically involves Cyclophosphamide, Cisplatin, Etoposide, and Vincristine. * **Retinoblastoma:** Often managed with systemic or intra-arterial chemotherapy using Vincristine, Etoposide, and Carboplatin (VEC regimen). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** Remember **"M"** for **M**elphalan and **"M"**ultiple **"M"**yeloma. * **Mechanism:** It is a cell cycle non-specific (CCNS) alkylating agent. * **Toxicity:** Like other nitrogen mustards, its dose-limiting toxicity is **bone marrow suppression** (myelosuppression) [2]. It also carries a risk of secondary malignancies (leukemogenic potential) with long-term use. * **Other uses:** It is occasionally used in Ovarian cancer and as part of Regional Perfusion for Malignant Melanoma.

Question 98: Which of the following anticancer drugs is NOT given intrathecally?

A. Methotrexate
B. Taxol (Correct Answer)
C. 5-Fluorouracil
D. Cyclophosphamide

Explanation: **Explanation:** The correct answer is **Taxol (Paclitaxel)**. Intrathecal (IT) administration is used to bypass the blood-brain barrier for treating or preventing meningeal leukemia or carcinomatosis. However, certain drugs are strictly contraindicated via this route due to severe **neurotoxicity**. **1. Why Taxol is the correct answer:** Taxanes like **Paclitaxel (Taxol)** and **Docetaxel** are highly neurotoxic. If administered intrathecally, they can cause devastating neurological damage, including seizures, encephalopathy, and permanent paralysis. Furthermore, their formulation (often containing Cremophor EL) is extremely irritating to the central nervous system. Other drugs strictly contraindicated for IT use include **Vincristine** (which is fatal if given IT) and **Anthracyclines**. **2. Analysis of Incorrect Options:** * **Methotrexate (A):** This is the most common drug used intrathecally. It is the gold standard for CNS prophylaxis in Acute Lymphoblastic Leukemia (ALL). * **5-Fluorouracil (C):** While less common than Methotrexate, 5-FU can be administered intrathecally in specific experimental or salvage protocols for neoplastic meningitis. * **Cyclophosphamide (D):** While the parent drug Cyclophosphamide is an inactive prodrug requiring hepatic activation (making IT use ineffective), it is not "contraindicated" in the same lethal sense as Taxol or Vincristine. However, in many clinical contexts, its active metabolite (Thiotepa) is preferred for IT use. *Note: In many standard textbooks, 5-FU and Cyclophosphamide are rarely used IT, but Taxol is the most definitive "never" among these options.* **High-Yield Clinical Pearls for NEET-PG:** * **Vincristine Warning:** Always remember: *"Vincristine is for Intravenous use only; Fatal if given by other routes."* It causes ascending myeloencephalopathy. * **Common IT Drugs:** The "Triple Intrathecal Therapy" usually consists of **Methotrexate, Cytarabine (Ara-C), and Hydrocortisone.** * **Liposomal Cytarabine:** Used for lymphomatous meningitis due to its extended half-life in the CSF.

Question 99: Which agent activates natural killer cells and is useful in renal cell carcinoma?

A. Aldesleukin (Correct Answer)
B. Etanercept
C. Leflunomide
D. Thalidomide

Explanation: Explanation: 1. Why Aldesleukin is correct: Aldesleukin is a recombinant form of Interleukin-2 (IL-2). Its primary mechanism involves promoting the proliferation and differentiation of T-cells and activating Natural Killer (NK) cells and Lymphokine-Activated Killer (LAK) cells [1]. These activated immune cells mount a potent anti-tumor response. Clinically, it is a high-yield treatment for Metastatic Renal Cell Carcinoma (RCC) and Malignant Melanoma. 2. Why the other options are incorrect: * Etanercept: This is a TNF-alpha inhibitor (a soluble decoy receptor). It is used in autoimmune conditions like Rheumatoid Arthritis and Psoriasis, not as an anticancer agent. * Leflunomide: An inhibitor of dihydroorotate dehydrogenase (DHODH), which blocks pyrimidine synthesis. It is a Disease-Modifying Antirheumatic Drug (DMARD) used primarily in Rheumatoid Arthritis. * Thalidomide: While used in Multiple Myeloma, its mechanism involves anti-angiogenesis and TNF-alpha inhibition, not the direct activation of NK cells for RCC [2]. 3. Clinical Pearls for NEET-PG: * Capillary Leak Syndrome: The most characteristic and life-threatening side effect of Aldesleukin/IL-2. It causes hypotension, edema, and multi-organ failure due to increased vascular permeability. * RCC Management: For NEET-PG, remember that while Aldesleukin is a classic answer, modern first-line treatments for RCC often involve Tyrosine Kinase Inhibitors (e.g., Sunitinib, Pazopanib) or Immune Checkpoint Inhibitors (e.g., Nivolumab) [3]. * Interferon-alpha: Another cytokine used in RCC, but its mechanism focuses more on increasing MHC expression and inhibiting viral replication/cell growth [1].

Question 100: Which chemotherapeutic agent is carcinogenic?

A. Alkylating agents (Correct Answer)
B. Antibiotics
C. Monoclonal antibodies
D. All of the above

Explanation: **Explanation:** **1. Why Alkylating Agents are the Correct Answer:** Alkylating agents (e.g., Cyclophosphamide, Busulfan, Melphalan) work by attaching an alkyl group to DNA, primarily at the N7 position of guanine. This causes DNA cross-linking and strand breaks. While this mechanism effectively kills rapidly dividing cancer cells, it is **non-specific**. If the damage occurs in healthy cells and is repaired incorrectly, it can lead to permanent mutations. Consequently, alkylating agents are known to be **leukemogenic** and **carcinogenic**. The most common secondary malignancy associated with their use is **Acute Myeloid Leukemia (AML)**, typically occurring years after treatment. **2. Why Other Options are Incorrect:** * **Antibiotics:** While some cytotoxic antibiotics (like Doxorubicin) can cause secondary malignancies due to topoisomerase II inhibition, as a class, they are primarily categorized by their cytotoxic/antitumor properties rather than being inherently classified as primary carcinogens in the same clinical context as alkylating agents. * **Monoclonal Antibodies:** These are targeted therapies (e.g., Rituximab, Trastuzumab) that bind to specific antigens. They do not directly damage DNA or cause mutations, thus they do not possess carcinogenic potential. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cyclophosphamide:** Associated with **Hemorrhagic Cystitis** (prevented by **MESNA**) and increased risk of **Transitional Cell Carcinoma** of the bladder. * **Busulfan:** High yield for causing **Pulmonary Fibrosis** ("Busulfan Lung") and skin hyperpigmentation. * **Nitrosoureas (Lomustine/Carmustine):** Highly lipid-soluble alkylating agents used for Brain Tumors (cross the BBB). * **Secondary Malignancy:** Always suspect a secondary AML in a patient previously treated for Hodgkin’s Lymphoma with alkylating-heavy regimens (like MOPP).

Practice by Chapter

Principles of Cancer Chemotherapy

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Alkylating Agents

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Antimetabolites

Practice Questions

Antitumor Antibiotics

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Plant Alkaloids

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Topoisomerase Inhibitors

Practice Questions

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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