Anticancer Drugs Practice Questions

Q: Which anticancer drug is known to cause cerebellar ataxia?

Cytarabine. **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)**.

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

Rituximab. ### 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).

Q: Which of the following is a proliferation signal inhibitor?

Sirolimus. **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).

Q: Siltuximab is used in the treatment of which condition?

Castleman disease. **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.

Q: All of the following are true about paclitaxel except?

Obtained from E. coli. **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."

Q: Melphalan is used in which of the following conditions?

Multiple myeloma. **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.

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

Aldesleukin. 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].

Q: Which chemotherapeutic agent is carcinogenic?

Alkylating agents. **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).

Question 1

Which anticancer drug is known to cause cerebellar ataxia?

Accepted Answer

Cytarabine

Answer

Cyclophosphamide

Answer

Chloramphenicol

Answer

Vinblastine

Question 2

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

Accepted Answer

Rituximab

Answer

Di-ethyl-stilbesterol

Answer

Tamoxifen

Answer

Bortezomib

Question 3

Which of the following is a proliferation signal inhibitor?

Accepted Answer

Sirolimus

Answer

Tacrolimus

Answer

Cyclosporine

Answer

None of the above

Question 4

Study light is caused by?

Accepted Answer

Alkylation agents

Answer

Vinca alkaloids

Answer

Antimetabolite

Answer

Antinomycin D

Question 5

Siltuximab is used in the treatment of which condition?

Accepted Answer

Castleman disease

Answer

Sézary syndrome

Answer

Ankylosing spondylitis

Answer

Non-Hodgkin lymphoma

Question 6

All of the following are true about paclitaxel except?

Accepted Answer

Obtained from E. coli

Answer

Stabilizes microtubules and prevents polymerization

Answer

Used in ovarian, cervix, and breast cancer

Answer

Most commonly causes myelosuppression and alopecia

Question 7

Melphalan is used in which of the following conditions?

Accepted Answer

Multiple myeloma

Answer

Wilm's tumour

Answer

Neuroblastoma

Answer

Retinoblastoma

Question 8

Which of the following anticancer drugs is NOT given intrathecally?

Accepted Answer

Taxol

Answer

Methotrexate

Answer

5-Fluorouracil

Answer

Cyclophosphamide

Question 9

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

Accepted Answer

Aldesleukin

Answer

Etanercept

Answer

Leflunomide

Answer

Thalidomide

Question 10

Which chemotherapeutic agent is carcinogenic?

Accepted Answer

Alkylating agents

Answer

Antibiotics

Answer

Monoclonal antibodies

Answer

All of the above

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

On this page

Practice by Chapter

Want unlimited practice?