Anticancer Drugs — MCQs

Anticancer Drugs Indian Medical PG Practice Questions and MCQs

Question 271: What grade of mucositis is characterized by large painful ulcers?

A. Grade 1
B. Grade 2
C. Grade 3 (Correct Answer)
D. Grade 4

Explanation: 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).

Question 272: Which of the following agents acts as a proteasome inhibitor?

A. Fludarabine
B. Thioguanine
C. Bortezomib (Correct Answer)
D. Rivaroxaban

Explanation: **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.

Question 273: Vismodegib is a new anticancer drug approved for the treatment of Basal Cell Carcinoma. It acts as an inhibitor of which pathway?

A. Hedgehog pathway (Correct Answer)
B. Poly ADP Ribose Polymerase
C. Cyclin Dependent Kinase-4
D. Her-2/neu

Explanation: **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.

Question 274: A patient receiving cisplatin, vinblastine, and bleomycin for a testicular neoplasm develops renal impairment. This is the effect of which drug(s)?

A. Cisplatin only (Correct Answer)
B. Bleomycin only
C. Vinblastine only
D. Both cisplatin and vinblastine

Explanation: **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).

Question 275: Which teratogen causes deafness?

A. Imatinib is used in the treatment of Chronic myelomonocytic leukemia (Correct Answer)
B. Imatinib is used in the treatment of MDS
C. Imatinib is used in the treatment of ALL
D. Imatinib is used in the treatment of GIST

Explanation: **Explanation:** The question asks for the clinical utility of **Imatinib**, a prototype tyrosine kinase inhibitor. **1. Why the Correct Answer is Right:** Imatinib is the first-line treatment for **Chronic Myeloid Leukemia (CML)** and is also FDA-approved for **Chronic Myelomonocytic Leukemia (CMML)** associated with rearrangements of the **PDGFR (Platelet-Derived Growth Factor Receptor)** gene. It works by inhibiting the BCR-ABL tyrosine kinase (in CML) and PDGFR kinase (in CMML), leading to the inhibition of abnormal cell proliferation. **2. Analysis of Incorrect Options:** * **Option B (MDS):** Myelodysplastic Syndromes are generally treated with hypomethylating agents like Azacitidine or Decitabine. Imatinib is not a standard treatment for MDS unless a specific PDGFR mutation is present (which overlaps with CMML). * **Option C (ALL):** While Imatinib is used in **Philadelphia chromosome-positive (Ph+) ALL**, it is not the primary treatment for ALL in general. However, in the context of this specific question, CMML/CML remains the more definitive association. * **Option D (GIST):** Imatinib is indeed used for **Gastrointestinal Stromal Tumors (GIST)** by inhibiting the **c-KIT tyrosine kinase**. (Note: If this were a "multiple correct" style question, D would also be correct; however, in many NEET-PG patterns, the most specific hematological indication is prioritized). **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Competitive inhibitor of the ATP-binding site on tyrosine kinase. * **Targets:** BCR-ABL, c-KIT, and PDGFR. * **Side Effects:** Most characteristic is **periorbital edema** (fluid retention). * **Resistance:** Most common cause is a point mutation in the BCR-ABL gene (e.g., **T315I mutation**), which requires drugs like Ponatinib. * **Teratogenicity:** Regarding the prompt's initial query, **Aminoglycosides** (e.g., Streptomycin) are the teratogens typically associated with **8th cranial nerve damage/deafness**.

Question 276: Which cell cycle specific anticancer drug acts mainly in the M phase of the cell cycle?

A. Cisplatin
B. Etoposide
C. Methotrexate
D. Paclitaxel (Correct Answer)

Explanation: **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).

Question 277: What is the mechanism of action of vincristine in the treatment of acute lymphoblastic leukemia (ALL)?

A. Inhibition of topoisomerase II to cause breaks in DNA strands
B. Alkylation and cross linking DNA strands
C. Inhibition of DNA mediated RNA synthesis
D. Inhibition of polymerization of tubulin to form microtubules (Correct Answer)

Explanation: **Mechanism of Action: Vincristine** **Correct Answer: D. Inhibition of polymerization of tubulin to form microtubules** **Explanation:** Vincristine is a **Vinca alkaloid** derived from the periwinkle plant (*Catharanthus roseus*). Its primary mechanism involves binding to **β-tubulin**, which inhibits its **polymerization** into microtubules [1], [3]. Microtubules are essential for the formation of the mitotic spindle during cell division. By preventing spindle formation, vincristine causes **mitotic arrest in the M-phase** (specifically metaphase), eventually leading to cell apoptosis [1], [3]. This makes it highly effective in rapidly dividing cells like those in Acute Lymphoblastic Leukemia (ALL) [2]. **Analysis of Incorrect Options:** * **Option A (Topoisomerase II Inhibition):** This is the mechanism of **Etoposide** and **Teniposide** (Epipodophyllotoxins), as well as Anthracyclines (like Doxorubicin). * **Option B (Alkylation/Cross-linking):** This describes **Alkylating agents** such as Cyclophosphamide, Ifosfamide, and Busulfan, which form covalent bonds with DNA. * **Option C (Inhibition of DNA-mediated RNA synthesis):** This is the mechanism of **Dactinomycin** (Actinomycin D), which intercalates into DNA to block transcription. **High-Yield Clinical Pearls for NEET-PG:** * **Cell Cycle Specificity:** Vincristine is **M-phase specific** [1]. * **Dose-Limiting Toxicity:** Unlike most anticancer drugs, Vincristine is **not** significantly bone marrow suppressive. Its dose-limiting toxicity is **Peripheral Neuropathy** (presents as "stocking-glove" anesthesia, loss of Achilles reflex, or paralytic ileus) [2]. * **Vincristine vs. Vinblastine:** Remember the mnemonic: **"Vincristine crisps the nerves (neurotoxicity); Vinblastine blasts the bone marrow (myelosuppression)."** * **Fatal Route:** Vincristine is for **Intravenous use only**. Intrathecal administration is fatal.

Question 278: Which enzyme is used as an anticancer drug?

A. L-asparaginase (Correct Answer)
B. Cytosine arabinoside
C. Methotrexate
D. Vincristine

Explanation: **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.

Question 279: Which of the following anticancer drugs acts by hypomethylation?

A. Gemcitabine
B. 5–FU
C. Decitabine (Correct Answer)
D. Homoharringtonine

Explanation: **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 280: Which of the following drugs has been recently approved for the treatment of prostate cancer?

A. Leuprolide
B. Goserelin
C. Abarelix
D. Degarelix (Correct Answer)

Explanation: **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.

Practice by Chapter

Principles of Cancer Chemotherapy

Practice Questions

Alkylating Agents

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Antimetabolites

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Antitumor Antibiotics

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Plant Alkaloids

Practice Questions

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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