Anticancer Drugs Practice Questions

Q: Practically all antineoplastic drugs can produce the following toxic effects except?

Cardiomyopathy. ### Explanation The core principle of traditional antineoplastic chemotherapy is the targeting of **rapidly dividing cells**. Most cytotoxic drugs are non-selective, affecting both malignant cells and normal tissues with high turnover rates. **Why Cardiomyopathy is the Correct Answer:** Cardiomyopathy is **not** a universal side effect of all anticancer drugs. It is a **drug-specific toxicity**, most notably associated with **Anthracyclines** (e.g., Doxorubicin, Daunorubicin) due to the generation of free radicals and lipid peroxidation in cardiac myocytes. Other examples of drug-specific toxicities include nephrotoxicity (Cisplatin), pulmonary fibrosis (Bleomycin), and hemorrhagic cystitis (Cyclophosphamide). **Analysis of Incorrect Options (Common Toxicities):** * **Depression of Leucocyte Count (Bone Marrow Suppression):** This is the most common dose-limiting toxicity. Since hematopoietic stem cells divide rapidly, they are highly susceptible to DNA-damaging agents. * **Mucositis:** The epithelial lining of the gastrointestinal tract (from the mouth to the anus) has a high turnover rate. Damage to these cells leads to painful inflammation and ulceration. * **Oligozoospermia:** Germinal epithelium in the testes is highly proliferative. Most cytotoxic drugs cause a decrease in sperm count, often leading to temporary or permanent sterility. **High-Yield Clinical Pearls for NEET-PG:** * **Exceptions to Bone Marrow Suppression:** Most drugs cause it, but **Vincristine, Bleomycin, and L-Asparaginase** are notable for being "bone marrow sparing." * **Doxorubicin Toxicity:** Acute toxicity presents as arrhythmias; chronic toxicity presents as **congestive heart failure (CHF)**. Dexrazoxane (an iron chelator) is used to prevent this. * **Emetic Potential:** Cisplatin is the drug with the highest emetic potential among anticancer agents.

Q: Which of the following agents acts as a proteasome inhibitor?

Bortezomib. **Explanation:** **Bortezomib** is the correct answer. It is a reversible inhibitor of the **26S proteasome**, a large protein complex responsible for degrading ubiquitinated proteins. By inhibiting the proteasome, Bortezomib prevents the degradation of pro-apoptotic proteins and inhibits the activation of **NF-κB** (Nuclear Factor kappa B). In normal cells, NF-κB promotes survival; its inhibition leads to apoptosis, particularly in plasma cells. This makes it a first-line agent for **Multiple Myeloma** and Mantle Cell Lymphoma. **Analysis of Incorrect Options:** * **A. Fludarabine:** A purine antimetabolite (analog of adenosine). it inhibits DNA polymerase and ribonucleotide reductase. It is primarily used in Chronic Lymphocytic Leukemia (CLL). * **B. Thioguanine:** A purine antimetabolite (6-TG) that incorporates into DNA/RNA to inhibit synthesis. It is used in Acute Myeloid Leukemia (AML). * **D. Rivaroxaban:** Not an anticancer drug. It is a **Direct Factor Xa inhibitor** (Oral Anticoagulant) used to prevent DVT and stroke in atrial fibrillation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Bortezomib contains **Boron**, which binds to the catalytic site of the proteasome. * **Adverse Effects:** The most characteristic side effect is **Peripheral Neuropathy** (often painful). It can also cause reactivation of Herpes Zoster (prophylactic acyclovir is often given). * **Other Proteasome Inhibitors:** Carfilzomib (irreversible) and Ixazomib (oral). * **Mnemonic:** Remember **"Bort-Myeloma"** – Bortezomib is the "gold standard" for Multiple Myeloma.

Q: Vismodegib is a new anticancer drug approved for the treatment of Basal Cell Carcinoma. It acts as an inhibitor of which pathway?

Hedgehog pathway. **Explanation:** **Vismodegib** is a first-in-class small molecule inhibitor specifically targeting the **Hedgehog (Hh) signaling pathway**. In normal physiology, this pathway is crucial for embryonic development, but its aberrant reactivation in adults is a primary driver of **Basal Cell Carcinoma (BCC)**. Vismodegib works by binding to and inhibiting **SMO (Smoothened)**, a transmembrane protein. By blocking SMO, the drug prevents the activation of GLI transcription factors, thereby halting the proliferation of tumor cells. It is primarily indicated for metastatic or locally advanced BCC where surgery or radiation is not feasible. **Analysis of Incorrect Options:** * **B. Poly ADP Ribose Polymerase (PARP):** Inhibitors like **Olaparib** and Niraparib are used for BRCA-mutated ovarian and breast cancers. They work by blocking DNA repair, leading to "synthetic lethality." * **C. Cyclin Dependent Kinase-4 (CDK4):** Inhibitors like **Palbociclib** and Ribociclib target the cell cycle (G1-S transition) and are used in HR-positive, HER2-negative breast cancer. * **D. Her-2/neu:** This is a receptor tyrosine kinase targeted by monoclonal antibodies like **Trastuzumab** or tyrosine kinase inhibitors like Lapatinib, primarily in breast and gastric cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** SMO Inhibitor (Hedgehog pathway). * **Key Indication:** Advanced/Metastatic Basal Cell Carcinoma (BCC). * **Gorlin Syndrome:** Also known as Nevoid BCC syndrome, it involves a mutation in the *PTCH1* gene (part of the Hh pathway), making these patients highly responsive to Vismodegib. * **Teratogenicity:** It is highly teratogenic (Category X); pregnancy must be strictly avoided. * **Common Side Effects:** Muscle spasms, dysgeusia (taste disturbance), and alopecia.

Q: A patient receiving cisplatin, vinblastine, and bleomycin for a testicular neoplasm develops renal impairment. This is the effect of which drug(s)?

Cisplatin only. **Explanation:** The correct answer is **Cisplatin only**. **1. Why Cisplatin is the correct answer:** Cisplatin is a platinum-based alkylating agent [1] notorious for its dose-limiting **nephrotoxicity**. It causes damage primarily to the proximal convoluted tubules (PCT) through oxidative stress and the formation of reactive oxygen species. This leads to a decrease in GFR and an increase in serum creatinine. To prevent this, patients are typically managed with aggressive **pre-treatment hydration** and the administration of **Amifostine** (a cytoprotective free-radical scavenger). **2. Why the other options are incorrect:** * **Bleomycin:** Its primary dose-limiting toxicity is **pulmonary fibrosis** (interstitial pneumonitis) [2]. It is unique among anticancer drugs for having minimal bone marrow suppression and no significant renal toxicity. * **Vinblastine:** As a microtubule inhibitor (Vinca alkaloid), its major dose-limiting toxicity is **bone marrow suppression** (specifically leukopenia). Its sister drug, Vincristine, is more associated with peripheral neuropathy. Neither causes renal impairment. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cisplatin Toxicities (Mnemonic: 3 N's):** **N**ephrotoxicity, **N**eurotoxicity (peripheral neuropathy), and **N**ausea/Vomiting (highly emetogenic). It is also **Ototoxic** (high-frequency hearing loss). * **Amifostine:** Specifically used to reduce cisplatin-induced nephrotoxicity. * **Testicular Cancer Regimen:** The combination used in the question is the **BEP regimen** (Bleomycin, Etoposide, Platinum/Cisplatin). * **Carboplatin:** A cisplatin analogue that is less nephrotoxic but more myelosuppressive (causes thrombocytopenia).

Q: Which enzyme is used as an anticancer drug?

L-asparaginase. **Explanation:** **1. Why L-asparaginase is the correct answer:** L-asparaginase is a unique chemotherapy agent because it is an **enzyme** derived from *E. coli* or *Erwinia chrysanthemi*. Its mechanism of action relies on a metabolic vulnerability in neoplastic cells (specifically in **Acute Lymphoblastic Leukemia/ALL**). Normal cells can synthesize the amino acid **L-asparagine** from aspartic acid using the enzyme *asparagine synthetase*. However, certain leukemic cells lack this enzyme and depend on exogenous (blood-borne) asparagine for protein synthesis. L-asparaginase catalyzes the conversion of circulating L-asparagine into aspartic acid and ammonia, effectively "starving" the cancer cells and leading to cell death. **2. Why the other options are incorrect:** * **B. Cytosine arabinoside (Ara-C):** This is an **antimetabolite** (pyrimidine analog) that inhibits DNA polymerase. * **C. Methotrexate:** This is an **antimetabolite** (folate antagonist) that inhibits the enzyme dihydrofolate reductase (DHFR). * **D. Vincristine:** This is a **vinca alkaloid** (mitotic inhibitor) that binds to tubulin and prevents microtubule polymerization. **3. NEET-PG High-Yield Pearls:** * **Clinical Use:** Primarily used in induction therapy for **Acute Lymphoblastic Leukemia (ALL)**. * **Major Side Effects:** Unlike most anticancer drugs, it is **not bone marrow suppressive**. Instead, it causes: * **Hypersensitivity reactions** (anaphylaxis) because it is a foreign bacterial protein. * **Acute Pancreatitis** (High-yield: look for abdominal pain in clinical vignettes). * **Hypofibrinogenemia** and clotting factor deficiencies leading to thrombosis or hemorrhage. * **Route:** Administered IM or IV.

Q: Which of the following anticancer drugs acts by hypomethylation?

Decitabine. **Explanation:** **Decitabine** (and its analog Azacitidine) is a pyrimidine antimetabolite that acts as a **DNA Methyltransferase (DNMT) inhibitor**. In many cancers, tumor suppressor genes are "silenced" through hypermethylation of their promoter regions. Decitabine incorporates into DNA and irreversibly binds to DNMTs, leading to **hypomethylation** (demethylation). This restores the normal expression of tumor suppressor genes, inducing cell differentiation and apoptosis. It is primarily used in Myelodysplastic Syndromes (MDS) and AML. **Analysis of Incorrect Options:** * **A. Gemcitabine:** A pyrimidine analog that inhibits **ribonucleotide reductase** and incorporates into DNA to cause chain termination. It is a mainstay for pancreatic and lung cancers. * **B. 5-Fluorouracil (5-FU):** A pyrimidine analog that inhibits **thymidylate synthase**, leading to "thymineless death" of the cell. It does not directly affect DNA methylation. * **D. Homoharringtonine (Omacetaxine):** A plant alkaloid that acts as a **protein synthesis inhibitor** by binding to the A-site of the ribosome and preventing the initial step of translation. It is used in CML. **High-Yield Clinical Pearls for NEET-PG:** * **Hypomethylating Agents:** Remember the duo—**Decitabine and Azacitidine**. * **Epigenetic Therapy:** These drugs are unique because they target "epigenetic" changes rather than direct DNA damage. * **Drug of Choice:** Decitabine is a high-yield answer for the management of **Myelodysplastic Syndrome (MDS)**. * **Side Effect:** Myelosuppression is the most common dose-limiting toxicity.

Q: Which of the following drugs has been recently approved for the treatment of prostate cancer?

Degarelix. **Explanation:** The correct answer is **Degarelix**. **1. Why Degarelix is correct:** Degarelix is a third-generation **GnRH (Gonadotropin-Releasing Hormone) receptor antagonist**. Unlike GnRH agonists, it binds competitively and reversibly to pituitary GnRH receptors, leading to an immediate suppression of LH and FSH. This results in a rapid drop in testosterone levels to castrate levels within 24–48 hours. Crucially, it **does not cause a "testosterone flare,"** making it highly effective for patients with advanced prostate cancer who require urgent androgen deprivation. **2. Why other options are incorrect:** * **A & B (Leuprolide and Goserelin):** These are **GnRH agonists**. While they are standard treatments for prostate cancer, they initially stimulate the pituitary, causing a transient surge in LH and testosterone (the "flare" phenomenon). This can worsen symptoms like bone pain or urinary obstruction unless co-administered with an anti-androgen (e.g., Flutamide). They are older, established drugs, not "recent" alternatives to antagonists. * **C (Abarelix):** Although Abarelix was the first GnRH antagonist approved, it was largely discontinued in many markets (including the US) due to a high risk of immediate-onset systemic hypersensitivity reactions. Degarelix has replaced it as the preferred antagonist. **Clinical Pearls for NEET-PG:** * **Mechanism:** GnRH Antagonists = Immediate suppression; GnRH Agonists = Initial surge followed by down-regulation. * **Testosterone Flare:** Always associate this risk with Leuprolide/Goserelin; it is avoided with Degarelix. * **Newer Drug Alert:** Keep an eye on **Relugolix**, which is the first *oral* GnRH antagonist approved for prostate cancer (FDA 2020). * **Side Effects:** Common to all androgen deprivation therapies are hot flashes, weight gain, and decreased libido.

Q: Which of the following drugs used in the therapy of metastatic melanoma is a MEK inhibitor?

Trametinib. **Explanation:** The treatment of metastatic melanoma often targets the **MAPK (Ras-Raf-MEK-ERK) signaling pathway**, which is constitutively active in about 50% of cases due to the **BRAF V600E mutation**. **Correct Option: D. Trametinib** Trametinib is a highly selective, reversible inhibitor of **MEK1 and MEK2** (Mitogen-activated extracellular signal-regulated kinase). By inhibiting MEK, it prevents the phosphorylation of ERK, thereby halting cell proliferation and inducing apoptosis in melanoma cells. It is frequently used in combination with Dabrafenib to delay the development of drug resistance. **Analysis of Incorrect Options:** * **A. Vemurafenib:** This is a selective inhibitor of the mutated **BRAF V600E kinase**. It acts upstream of MEK. * **B. Ipilimumab:** This is a **CTLA-4 inhibitor** (checkpoint inhibitor). It works by enhancing the T-cell mediated immune response against tumor cells rather than targeting intracellular signaling pathways. * **C. Dabrafenib:** Similar to Vemurafenib, this is a **BRAF inhibitor**. **High-Yield Clinical Pearls for NEET-PG:** * **The "Nib" vs. "Mab" Rule:** Small molecule inhibitors end in "-nib" (kinase inhibitors), while monoclonal antibodies end in "-mab". * **Combination Therapy:** Combining a BRAF inhibitor (Dabrafenib) with a MEK inhibitor (Trametinib) is superior to monotherapy because it reduces the incidence of secondary skin cancers (like squamous cell carcinoma) caused by paradoxical MAPK pathway activation. * **Other MEK Inhibitors:** Cobimetinib and Binimetinib. * **Key Side Effect:** MEK inhibitors are uniquely associated with **acneiform rash** and **retinal vein occlusion**.

Question 1

Practically all antineoplastic drugs can produce the following toxic effects except?

Accepted Answer

Cardiomyopathy

Answer

Depression of leucocyte count

Answer

Mucositis

Answer

Oligozoospermia

Question 2

Which of the following agents acts as a proteasome inhibitor?

Accepted Answer

Bortezomib

Answer

Fludarabine

Answer

Thioguanine

Answer

Rivaroxaban

Question 3

Vismodegib is a new anticancer drug approved for the treatment of Basal Cell Carcinoma. It acts as an inhibitor of which pathway?

Accepted Answer

Hedgehog pathway

Answer

Poly ADP Ribose Polymerase

Answer

Cyclin Dependent Kinase-4

Answer

Her-2/neu

Question 4

A patient receiving cisplatin, vinblastine, and bleomycin for a testicular neoplasm develops renal impairment. This is the effect of which drug(s)?

Accepted Answer

Cisplatin only

Answer

Bleomycin only

Answer

Vinblastine only

Answer

Both cisplatin and vinblastine

Question 5

Which teratogen causes deafness?

Accepted Answer

Imatinib is used in the treatment of Chronic myelomonocytic leukemia

Answer

Imatinib is used in the treatment of MDS

Answer

Imatinib is used in the treatment of ALL

Answer

Imatinib is used in the treatment of GIST

Question 6

What is the mechanism of action of vincristine in the treatment of acute lymphoblastic leukemia (ALL)?

Accepted Answer

Inhibition of polymerization of tubulin to form microtubules

Answer

Inhibition of topoisomerase II to cause breaks in DNA strands

Answer

Alkylation and cross linking DNA strands

Answer

Inhibition of DNA mediated RNA synthesis

Question 7

Which enzyme is used as an anticancer drug?

Accepted Answer

L-asparaginase

Answer

Cytosine arabinoside

Answer

Methotrexate

Answer

Vincristine

Question 8

Which of the following anticancer drugs acts by hypomethylation?

Accepted Answer

Decitabine

Answer

Gemcitabine

Answer

5–FU

Answer

Homoharringtonine

Question 9

Which of the following drugs has been recently approved for the treatment of prostate cancer?

Accepted Answer

Degarelix

Answer

Leuprolide

Answer

Goserelin

Answer

Abarelix

Question 10

Which of the following drugs used in the therapy of metastatic melanoma is a MEK inhibitor?

Accepted Answer

Trametinib

Answer

Vemurafenib

Answer

Ipilimumab

Answer

Dabrafenib

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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