Anticancer Drugs Practice Questions

Q: Which of the following statements about Trastuzumab is FALSE?

It causes upregulation of HER2/neu.. ### Explanation **Trastuzumab** is a recombinant humanized monoclonal antibody specifically targeting the extracellular domain of the **HER2/neu (ErbB2)** receptor, which is overexpressed in approximately 25–30% of breast cancer cases. **Why Option C is False (The Correct Answer):** Trastuzumab works by binding to the HER2 receptor, leading to its **downregulation** (internalization and degradation of the receptor) rather than upregulation. It also inhibits receptor dimerization, prevents the cleavage of the extracellular domain, and induces **Antibody-Dependent Cellular Cytotoxicity (ADCC)** via Natural Killer (NK) cells. **Analysis of Other Options:** * **Option A:** Trastuzumab shows a synergistic effect when combined with taxanes like **Paclitaxel**. This combination significantly improves response rates and survival compared to monotherapy. * **Option B:** It is a standard-of-care treatment for **metastatic breast cancer** and is also used in the adjuvant setting for HER2-positive early-stage breast cancer and metastatic gastric adenocarcinoma. * **Option D:** Unlike traditional cytotoxic chemotherapy, Trastuzumab is a targeted therapy and **does not cause significant bone marrow suppression** (myelosuppression) or alopecia. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiotoxicity:** The most significant side effect is **reversible cardiomyopathy** (decrease in Left Ventricular Ejection Fraction). Unlike Doxorubicin, it is not dose-dependent and does not show "Anthracycline-like" vacuolar degeneration. * **Contraindication:** It should generally **not** be administered concurrently with Anthracyclines (like Doxorubicin) due to an increased risk of heart failure. * **Monitoring:** Baseline and periodic **Echocardiography (MUGA scan)** is mandatory.

Q: What grade of mucositis is characterized by large painful ulcers?

Grade 3. Oral mucositis is a common and debilitating side effect of chemotherapy (e.g., Methotrexate, 5-Fluorouracil) and radiotherapy. The World Health Organization (WHO) grading system is the gold standard for classification, focusing on the presence of ulcers and the patient's ability to eat. **Explanation of the Correct Answer:** * **Grade 3 (Correct):** This stage is characterized by **extensive, painful ulcerations and erythema**. Clinically, the patient is **unable to swallow solid food** and is restricted to a liquid diet. The presence of "large painful ulcers" that significantly impair oral intake is the hallmark of Grade 3. **Analysis of Incorrect Options:** * **Grade 1:** Characterized by soreness and erythema (redness) of the mucosa, but **no ulcers** are present. * **Grade 2:** Characterized by erythema and **small, isolated ulcers**. The patient can still swallow solid food despite the discomfort. * **Grade 4:** This is the most severe stage where oral intake is impossible. The patient requires **total parenteral nutrition (TPN)** or enteral feeding due to the severity of the lesions. **NEET-PG High-Yield Pearls:** * **Drug Association:** Methotrexate is a classic cause of mucositis. **Folinic acid (Leucovorin)** is used as a "rescue" to prevent/limit this toxicity. * **Management:** Palifermin (Recombinant Human Keratinocyte Growth Factor) is used to reduce the incidence and duration of severe mucositis in patients receiving high-dose chemotherapy. * **Quick Recall Table:** * Grade 1: Erythema only. * Grade 2: Ulcers + Can eat solids. * Grade 3: Ulcers + Liquid diet only. * Grade 4: No oral intake possible (TPN required).

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 cell cycle specific anticancer drug acts mainly in the M phase of the cell cycle?

Paclitaxel. **Explanation:** The correct answer is **Paclitaxel**. Anticancer drugs are classified into Cell Cycle Specific (CCS) and Cell Cycle Non-Specific (CCNS) agents. **1. Why Paclitaxel is correct:** Paclitaxel belongs to the **Taxane** group. Its mechanism of action involves binding to the $\beta$-tubulin subunit, which **promotes microtubule assembly** and stabilizes them against depolymerization. This "freezes" the microtubules, preventing the formation of the mitotic spindle required for sister chromatid separation. Consequently, the cell is arrested in the **M phase (Mitosis)**, leading to apoptosis. **2. Why other options are incorrect:** * **Cisplatin:** It is a **Cell Cycle Non-Specific (CCNS)** agent. It acts by forming intra-strand cross-links in DNA, interfering with replication regardless of the cell cycle phase. * **Etoposide:** This is a CCS drug, but it acts specifically in the **late S to G2 phase** by inhibiting Topoisomerase II, leading to DNA strand breaks. * **Methotrexate:** This is an antimetabolite that inhibits Dihydrofolate Reductase (DHFR). It is highly specific for the **S phase** (DNA synthesis phase). **3. NEET-PG High-Yield Pearls:** * **M-Phase Specific Drugs:** Remember the mnemonic **"Vincas and Taxanes."** While Vinca alkaloids (Vincristine/Vinblastine) *prevent* microtubule assembly, Taxanes *prevent* disassembly. * **G2-Phase Specific:** Bleomycin and Etoposide. * **S-Phase Specific:** Antimetabolites (5-FU, Methotrexate, Cytarabine) and Hydroxyurea. * **Side Effect Note:** Paclitaxel is notorious for causing peripheral neuropathy and hypersensitivity reactions (pre-medicate with dexamethasone and antihistamines).

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.

Question 1

Which of the following statements about Trastuzumab is FALSE?

Accepted Answer

It causes upregulation of HER2/neu.

Answer

It shows better response in combination with paclitaxel.

Answer

It is used in metastatic breast cancer.

Answer

It does not cause bone marrow toxicity.

Question 2

What grade of mucositis is characterized by large painful ulcers?

Accepted Answer

Grade 3

Answer

Grade 1

Answer

Grade 2

Answer

Grade 4

Question 3

Which of the following agents acts as a proteasome inhibitor?

Accepted Answer

Bortezomib

Answer

Fludarabine

Answer

Thioguanine

Answer

Rivaroxaban

Question 4

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 5

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 6

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 7

Which cell cycle specific anticancer drug acts mainly in the M phase of the cell cycle?

Accepted Answer

Paclitaxel

Answer

Cisplatin

Answer

Etoposide

Answer

Methotrexate

Question 8

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 9

Which enzyme is used as an anticancer drug?

Accepted Answer

L-asparaginase

Answer

Cytosine arabinoside

Answer

Methotrexate

Answer

Vincristine

Question 10

Which of the following anticancer drugs acts by hypomethylation?

Accepted Answer

Decitabine

Answer

Gemcitabine

Answer

5–FU

Answer

Homoharringtonine

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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